<?xml version="1.0" encoding="UTF-8" ?>
<rdf:RDF xmlns:admin="http://webns.net/mvcb/" xmlns="http://purl.org/rss/1.0/" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:prism="http://purl.org/rss/1.0/modules/prism/" xmlns:taxo="http://purl.org/rss/1.0/modules/taxonomy/" xmlns:content="http://purl.org/rss/1.0/modules/content/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:syn="http://purl.org/rss/1.0/modules/syndication/">
<channel rdf:about="https://biorxiv.org">
<admin:errorReportsTo rdf:resource="mailto:biorxiv@cshlpress.edu"/>
<title>bioRxiv Subject Collection: Genetics Plant Biology</title>
<link>https://biorxiv.org</link>
<description>
This feed contains articles for bioRxiv Subject Collection "Genetics Plant Biology"
</description>

<items>
<rdf:Seq>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.09.730892v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.09.731144v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.09.731016v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.08.730759v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.09.731195v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.08.730950v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.09.730991v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.08.730940v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.10.731310v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.08.730986v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.10.731306v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.09.730678v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.09.729629v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.07.730721v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.07.724338v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.08.730819v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.06.730570v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.05.730474v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.06.730627v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.07.730749v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.09.731113v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.09.731038v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.10.731257v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.08.730374v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.08.730953v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.08.730856v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.08.730999v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.06.730605v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.07.730737v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.06.09.731087v1?rss=1"/>
</rdf:Seq>
</items>
<prism:eIssn/>
<prism:publicationName>bioRxiv</prism:publicationName>
<prism:issn/>

<image rdf:resource=""/>
</channel>
<image rdf:about="">
<title>bioRxiv</title>
<url>https://www.biorxiv.org/sites/default/files/bioRxiv_article.jpg</url>
<link>https://www.biorxiv.org</link>
</image>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.09.730892v1?rss=1">
<title>
<![CDATA[
The Iberian white-oak syngameon as a legacy of introgression in southern Europe 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.09.730892v1?rss=1
</link>
<description><![CDATA[
Oaks (Quercus L.) are among the most ecologically important tree genera in the northern hemisphere, with an intricate evolutionary history reflected in a reticulated phylogeny. Oak diversity has been profoundly shaped by introgression and diversification, yet the Iberian Peninsula remains an understudied natural laboratory for understanding these evolutionary processes. We used RAD-seq to characterize 38 taxa (including nothotaxa) and investigate the evolutionary history of the Iberian white oaks, with an emphasis on hybrid swarms. Results led to a readdressing of Iberian white oak species, expanding our current understanding of the phylogeography of the European Section Quercus. Furthermore, molecular evidence led to the circumscription of two new subsections, reflecting the contrast between typical temperate and Atlantic distributed species (Group A), and the submediterranean marcescent oaks (Group B). The former unveiled the recovery of Q. estremadurensis and a Northwestern Iberian lineage represented by Q. broteroana and Q. orocantabrica as southwestern representatives of the broad European pedunculate oaks (Q. robur s.l.). The latter led to the validation of hybrid swarms, emphasizing the Iberian oak syngameon and the importance of gene flow to oak evolution. Ultimately, our approach advances the understanding of European white oak evolution across different evolutionary scales, establishing the Iberian Peninsula as an important reservoir of oak diversity.
]]></description>
<dc:creator><![CDATA[ Vila-Vicosa, C. M., Castilho, R., Vazquez, F. M. P., Almeida, R. S., Garcia, C. P., Pereira, A. B., Hipp, A., Avezedo, H. ]]></dc:creator>
<dc:date>2026-06-11</dc:date>
<dc:identifier>doi:10.64898/2026.06.09.730892</dc:identifier>
<dc:title><![CDATA[The Iberian white-oak syngameon as a legacy of introgression in southern Europe]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-11</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.09.731144v1?rss=1">
<title>
<![CDATA[
Insights into the genetic architecture of resistance to viral haemorrhagic septicaemia virus in rainbow trout from a genome-wide association study to in vitro CRISPR-Cas9 functional evaluation 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.09.731144v1?rss=1
</link>
<description><![CDATA[
Viral haemorrhagic septicaemia (VHS) is a severe disease affecting rainbow trout (Oncorhynchus mykiss) and a wide range of wild freshwater and marine fish species. VHSV threatens rainbow trout aquaculture, as it may cause 100% mortality in fry. Previous studies identified a quantitative trait locus (QTL) on chromosome 3 associated with resistance to VHSV waterborne challenge and reduced viral replication in fin explants, although these findings were obtained using limited genetic diversity. The objective of this study was to validate and extend the identification of genomic regions associated with resistance to VHSV in the genetically diverse rainbow trout line designated synthetic. A genome-wide association study (GWAS) was conducted using whole-genome sequences from parents of progeny classified as resistant or susceptible to a VHSV waterborne challenge. While the QTL on chromosome 3 was not validated in the synthetic line, four novel suggestive SNPs associated with survival following VHSV waterborne challenge were identified on chromosomes 6, 8, 17, and 32. Notably, one SNP on chromosome 17 was located within a gene potentially involved in antiviral defence, a paralog of lrp1 (low-density lipoprotein receptor-related protein 1). To further investigate its role, lrp1 function was analysed in vitro using CRISPR-Cas9 genome editing. Three independent lrp1-/- CHSE-EC cell lines were generated and challenged with VHSV. The results showed that lrp1 is not essential for viral entry but may modulate the inflammatory response during VHSV infection in epithelial cell lines.
]]></description>
<dc:creator><![CDATA[ Thomas, V., Collet, B., Quillet, E., Marchand, M., Huetz, F., Boudinot, P., Phocas, F., Lallias, D. ]]></dc:creator>
<dc:date>2026-06-11</dc:date>
<dc:identifier>doi:10.64898/2026.06.09.731144</dc:identifier>
<dc:title><![CDATA[Insights into the genetic architecture of resistance to viral haemorrhagic septicaemia virus in rainbow trout from a genome-wide association study to in vitro CRISPR-Cas9 functional evaluation]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-11</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.09.731016v1?rss=1">
<title>
<![CDATA[
Host genetic regulation of fermentation-related cecal microbial taxa is associated with loin muscle deposition in meat rabbits 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.09.731016v1?rss=1
</link>
<description><![CDATA[
Loin muscle weight is an important indicator of carcass yield in meat rabbit production, but the host genetic and intestinal microbial factors associated with its variation remain poorly understood. Because the cecum is the primary site of hindgut fermentation in rabbits, we integrated whole-genome resequencing, cecal transcriptome profiling, and cecal and rectal 16S rRNA sequencing data from 321 Kangda meat rabbits, with rectal microbiome data used as a downstream comparative reference. Compared with the rectum, the cecum contained a richer microbial community, with more ASVs and genera and significantly higher microbial diversity, whereas predicted metabolic functions were largely conserved between the two segments. Loin muscle weight showed moderate SNP-based heritability (h2= 0.39), and the cecal microbiome explained a smaller but detectable proportion of phenotypic variation (m2 = 0.13). Multi-strategy microbial screening identified 19 candidate cecal genera associated with loin muscle weight, with Methanosphaera showing the strongest negative association. Host GWAS prioritized candidate loci near MEX3C and TCF4 on chromosome 10, and integration of cecal cis-eQTL and GWAS summary statistics further prioritized GJB3 as a candidate gene associated with loin muscle weight. Consistent with the cecum-centered model, host genetic relatedness was weakly but significantly correlated with cecal microbial similarity, whereas no such global association was observed for the rectal microbiome. Microbial GWAS and SMR analyses further prioritized a cecal MRAP2-Methanobrevibacter association as the main host-regulated microbial signal, while rectal analyses identified distinct segment-specific signals, including SULF1-Roseburia. These findings suggest that host genetic variation may be linked to loin muscle deposition partly through cecal gene expression and fermentation-related cecal microbial taxa, with the rectal microbiome providing comparative evidence for hindgut segment specificity. This study provides candidate host and microbial targets for future functional validation and microbiome-informed nutritional strategies to improve carcass traits in meat rabbits.
]]></description>
<dc:creator><![CDATA[ Di, Y., Fu, Q., Xie, K., Song, Z., Li, W., Li, X., Zhang, Q., Ning, C., Wang, D., Fan, X. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.09.731016</dc:identifier>
<dc:title><![CDATA[Host genetic regulation of fermentation-related cecal microbial taxa is associated with loin muscle deposition in meat rabbits]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.08.730759v1?rss=1">
<title>
<![CDATA[
Uncovering Pseudotime-Varying Genetic Causal Effects Along Single-Cell Trajectories for Pulmonary Disease Trait 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.08.730759v1?rss=1
</link>
<description><![CDATA[
With the increasing accessibility of single-cell RNA sequencing (scRNA-seq) data, cell-type-specific gene expression can be linked to complex traits through pseudo-bulk method, which considered aggregated gene expression from multiple cells of the same annotated cell type per individual and clearly shows the limitation of ignoring intra-individual cell-to-cell variability. Concurrently, pseudotime trajectory inference has gained popularity for its ability to capture continuous biological processes such as cell differentiation and lineage development, instead of individual discrete stages. It is natural to consider whether genetic effects for complex traits, such as individual level disease status, show a dynamic pattern along the inferred trajectories. In this study, we introduce a novel framework that models gene expression as a function of pseudotime along the inferred trajectories. We mapped expression quantitative trait loci (eQTL) effects in the cis-region as functional parameters, which we called "dynamic eQTLs", showing regulatory effects exerted by genetic variants change continuously along the cellular trajectory. For eQTLs of constant effects across pseudotime we leveraged external bulk-eQTL information to enhance the power. Furthermore, we employed significant, variable dynamic eQTLs as instrumental variables to infer causal relationships between gene expression and complex traits. To address challenges inherent to scRNA-seq data - such as sparsity and high variability - we incorporate an empirical likelihood-based inference method, which is non-parametric and self-normalized. Besides, genes associated with trajectory branchpoints may bring confounding, and we also proposed a causal mediation analysis framework to determine whether a gene plays a causal role for the disease directly and indirectly through driving cell fates. Applying our method to scRNA-seq data from human lung tissue of 114 samples (66 pulmonary fibrosis cases and 48 controls), along with meta-analyzed GWAS summary statistics for IPF from 3 studies, we identified pseudotime-dependent causal effects for IPF from genes implicated in the trajectory AT2 -translational AT2 - AT1, which is crucial in lung tissue repair and regeneration. We also found that 30 genes have a mediated effect through cell fates.
]]></description>
<dc:creator><![CDATA[ Chen, S., Moorthy, A., Yu, P. K., Wang, J., Liu, D. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.08.730759</dc:identifier>
<dc:title><![CDATA[Uncovering Pseudotime-Varying Genetic Causal Effects Along Single-Cell Trajectories for Pulmonary Disease Trait]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.09.731195v1?rss=1">
<title>
<![CDATA[
TOMM40 '523' genotype induces sex- and tissue- specific differences in cholesterol and triglyceride levels in an APOE-TOMM40 humanized mouse model 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.09.731195v1?rss=1
</link>
<description><![CDATA[
Introduction: Genetic variants within the APOE-TOMM40 locus are associated with Alzheimer's disease (AD). A specific role for TOMM40 is indicated by the finding that '523' poly-T variants are associated with AD risk, but the mechanism for this effect has not been established. Our studies have shown that suppression of Tomm40 in mice increased brain cholesterol content, an AD risk factor, and thus the present study sought to assess whether major '523' poly-T variants (Short [S] and Very Long [VL]) are associated with altered lipid content of brain and other tissues. Methods: We utilized a mouse model containing the entire human APOE3-TOMM40 locus to quantify cholesterol and triglyceride levels in brain, liver, and white adipose tissue (WAT), as well as brain content of the AD biomarkers A{beta} 42 and tau, in mice carrying two homozygous TOMM40 '523' poly-T genotypes (S/S and VL/VL). Results: Male mice carrying the '523'-S/S genotype, but not females, showed higher brain cholesterol and triglyceride levels than VL/VL carriers, together with greater brain A{beta} 42 content. WAT showed similar lipid differences as in the brain, while hepatic lipid content was broadly similar between '523'-S/S and -VL/VL genotypes, though there was a trend for higher triglycerides in VL/VL mice in a sex- and age- dependent manner. Discussion: These results demonstrate that TOMM40 '523' poly-T variants drive tissue-specific, sex-, and age-dependent lipid differences in humanized APOE3-TOMM40 mice, with the S/S genotype linked to elevated brain cholesterol and A{beta} 42 levels, effects that link this locus to AD pathogenesis.
]]></description>
<dc:creator><![CDATA[ Yang, N. V., Hodgson, D., Jang, T. M., Kim, J. J., Gottschalk, W. K., Yassine, H. N., Chiba-Falek, O., Krauss, R. M. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.09.731195</dc:identifier>
<dc:title><![CDATA[TOMM40 '523' genotype induces sex- and tissue- specific differences in cholesterol and triglyceride levels in an APOE-TOMM40 humanized mouse model]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.08.730950v1?rss=1">
<title>
<![CDATA[
Two SID-1-dependent genes sensitive to heritable epigenetic changes can also impact reproduction 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.08.730950v1?rss=1
</link>
<description><![CDATA[
Import of double-stranded RNA (dsRNA) into the germ line can have consequences that last for many generations. However, the role of such transgenerational regulation by extracellular dsRNA is unclear. In the nematode C. elegans, entry of dsRNA into the cytosol requires the transmembrane protein SID-1 and loss of SID-1 for a few generations causes changes in gene expression that can persist for hundreds of generations. Here we report an expanded number of such SID-1-dependent genes (SDGs) and analyze two germline-expressed SDGs: sdg-1 and sdg-2. Deleting sdg-1 reduces brood size in some lineages. An endogenous SDG-1::mCherry fusion protein shows conditional enrichment within nuclei, colocalization with perinuclear germ granules, and colocalization with microtubules. Although animals with SDG-1::mCherry have a normal brood size, they have fewer early progeny with some animals showing defective germline morphology. Deleting the sdg-1 open reading frame eliminates defects in most but not all the animals that express mCherry in a now sdg-1(-) background, suggesting transgenerational consequences of SDG-1::mCherry that persist in some siblings lacking sdg-1. Deleting sdg-2 also reduces brood size in some lineages. An endogenous SDG-2::mCherry fusion protein is constitutively detectable in the cytoplasm and nucleus. The sequence and predicted structure of SDG-2 suggest that it can interact with the Gli-type transcription factor TRA-1, which regulates spermatogenesis. Together, these results suggest that changes in SDG-1 or SDG-2 can impact reproduction. Therefore, the import of extracellular dsRNA or other SID-1 function(s) that regulate SDGs could have evolved to modulate the lingering impacts of ancestral epigenetic changes.
]]></description>
<dc:creator><![CDATA[ Sathya, A., Shugarts Devanapally, N. M., Yi, A. L., Jose, A. M. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.08.730950</dc:identifier>
<dc:title><![CDATA[Two SID-1-dependent genes sensitive to heritable epigenetic changes can also impact reproduction]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.09.730991v1?rss=1">
<title>
<![CDATA[
Inference of elevated mutation rates and variant effects using 700k exomes 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.09.730991v1?rss=1
</link>
<description><![CDATA[
Genomic sequencing is now widely accessible for genetic diagnostics and is emerging as a component of newborn screening. This technological development generates the need to characterize incoming mutations, create comprehensive datasets of genes causing rare Mendelian disorders, and identify pathogenic variants. Large-scale exome sequencing datasets such as Genome Aggregation Database (gnomAD) have been assembled to help address these challenges. The recent release of gnomAD (v4; n = 730,947) uncovers millions of rare coding variants, many of which have arisen more than once by independent recurrent mutations in the rapidly growing recent human population. Here, we use newly developed theoretical understanding of sampling properties of rare variants to estimate key population genetics parameters of practical importance to human genetics such as demography history, mutation rate, and selection. Solely relying on population data, our method Population Inferred Estimates of Selection (PIES) identifies novel genes with loss-of-function mutational hotspots likely due to selection in spermatogonia. PIES efficiently estimates selection coefficients for heterozygous loss-of-function variants. Combining population genetics inference with variant effect predictors, PIES predicts pathogenic missense mutations and improves variant prioritization for genetic diagnostics and newborn screening.
]]></description>
<dc:creator><![CDATA[ Kar, P., Moldovan, M. A., Guez, J., Nazeen, S., Goodrich, J. K., Karani, T., Samocha, K. E., Karczewski, K., Koch, E., Seplyarskiy, V., Sunyaev, S. R. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.09.730991</dc:identifier>
<dc:title><![CDATA[Inference of elevated mutation rates and variant effects using 700k exomes]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.08.730940v1?rss=1">
<title>
<![CDATA[
Somatic CRISPR editing of Msh3 mitigates Huntington's disease pathology in mice 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.08.730940v1?rss=1
</link>
<description><![CDATA[
Huntington's disease (HD) is a fatal, dominantly inherited neurodegenerative disorder caused by a CAG repeat expansion in Huntingtin (HTT) exon 1. Further progressive CAG repeat expansion occurs in somatic cells, particularly in neurons, and drives the timing of clinical onset. Therefore, therapeutic strategies to slow somatic expansion are predicted to be disease-modifying. Somatic CAG expansion is driven by mismatch repair protein MSH3, a leading therapeutic target supported by human genetic data. To gain insight into the impact of targeting MSH3 at different stages of the disease process we used somatic CRISPR-Cas9 editing to knock out Msh3 in HttQ111 mice at ages of 6, 16, 24 weeks exhibiting progressively increasing somatic expansion. Intervention at all three ages slowed striatal CAG expansion, reduced nuclear huntingtin pathology and suppressed transcriptional dysregulation, with earlier intervention having greater impact. Msh3 knockout also suppressed the production of the exon 1 Htt1a transcript. The results of our study provide important preclinical information relevant to an MSH3 therapeutic in humans that would be expected to impact a subset of cells in the brain, provide insight into the influence of timing of intervention on therapeutic effectiveness and deepen our understanding of how targeting MSH3 could alter the trajectory of HD.
]]></description>
<dc:creator><![CDATA[ Oliver, E., Kovalenko, M., Louca, M., Jiang, A., Westerdahl, J., Correia, K., Jones, B., Saif, F., Romano, N., Sidhu, A., Gillis, T., Elezi, E., Murtha, R., Mouro Pinto, R., Wheeler, V. C. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.08.730940</dc:identifier>
<dc:title><![CDATA[Somatic CRISPR editing of Msh3 mitigates Huntington's disease pathology in mice]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.10.731310v1?rss=1">
<title>
<![CDATA[
POISE: Spectral Inference of Parent-of-Origin Effects in Unlabeled Genomic Data 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.10.731310v1?rss=1
</link>
<description><![CDATA[
Motivation: Parent of Origin Effects (POEs), where the effect of an an allele on a phenotype differs based on maternal or paternal inheritance implicated in growth, metabolism, and neurodevelopment. Traditional tests for POEs require family data to determine parental origins of transmitted alleles. Given that such studies are expensive and time consuming compared to genome-wide association studies (GWAS), tests that function absent inheritance information are highly desirable. We develop a method, based on community detection from machine learning, that infers POEs via a spectral decomposition, obtains confidence intervals via a non-parametric bootstrap, and safeguards against confounding by non POE sources of variation. We refer to our method as Parent of Origin Inference via Spectral Estimation (POISE). Results: We demonstrate that POISE is well-calibrated under both Gaussian and heavy-tailed noise in simulation studies, with improved robustness to true POEs compared to existing covariance-based tests. POISE provides per-trait effect estimates with bias-corrected bootstrap confidence intervals and incorporates an information-theoretic minimum detectable effect size that filters unreliable estimates, conferring robustness to covariance-deflating variance QTL. We then apply POISE to GWAS data from the UK Biobank using BMI, LDL cholesterol, and HDL cholesterol. POISE recovers established POE loci and identifies 134 additional variants at genes implicated in lipid metabolism, immune regulation, and growth. Availability and implementation: The code for this method in Python is available at https://github.com/bystrogenomics/POISE.
]]></description>
<dc:creator><![CDATA[ Hwang, I., Talbot, A., Head, T., Trevino, C., Wingo, T. S., Kotlar, A. V. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.10.731310</dc:identifier>
<dc:title><![CDATA[POISE: Spectral Inference of Parent-of-Origin Effects in Unlabeled Genomic Data]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.08.730986v1?rss=1">
<title>
<![CDATA[
Duplication of superoxide dismutase and a mutation in aquaglyceroporin mediates the sensitivity of Plasmodium falciparum to cryptosporin, a natural product derived from Acaromyces ingoldii 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.08.730986v1?rss=1
</link>
<description><![CDATA[
Cryptosporin, a fungal metabolite, exhibited potent antimalarial activity against both asexual blood stage Plasmodium falciparum and liver-stage Plasmodium berghei with minimal human HepG2 toxicity. Unlike atovaquone, the mechanism of cryptosporin is independent of mitochondrial electron transport. Minimum inoculum of resistance showed a low risk of resistance development. RNA-Seq analysis revealed the upregulation of genes associated with sexual development including many canonical markers such as Pfs25, and PfCCp3, suggesting a stress response that is also seen when parasites are treated with artemisinin. In vitro evolution and whole genome sequencing analysis identified a mutation (F138Y) in PfAQP (PF3D7_1132800) and duplications of the two superoxide dismutase genes, PfSOD-1 (PF3D7_0814900) and PfSOD-2 (PF3D7_0623500). CRISPR/Cas9 editing confirmed that the F138Y mutation in PfAQP was sufficient to confer resistance to cryptosporin. Alignment of the P. falciparum structure with that of HsAQP3 suggests the mutation may impact transport of hydrogen peroxide and the transition between open and closed conformations. Indeed, studies with BY4742 yeast lacking fps1 but expressing PfAQP showed that the permeability of PfAQP was not affected by cryptosporin and that it is likely not a direct target. Taken together, this study highlights the role of PfAQP in the resistance development of cryptosporin. In addition, cryptosporin likely induces high levels of oxidative stress which results in the duplications of oxidative dismutase genes as part of the parasite defense response. These findings highlight the role of PfAQP in mediating drug resistance, the mechanism of which warrants further research.
]]></description>
<dc:creator><![CDATA[ Jiang, T., Collins, J. E., Lee, J. W., Buss, S., Thommen, B. T., Edgar, R. C. S., Wendt, K., Chen, D. W., Li, C., Mittal, N., Paes, R., Santos, N. M., Ferreira, L. T., Bhasin, J., Momper, J. D., Fidock, D. A., Lee, M., Duraisingh, M. T., Beitz, E., Cichewicz, R. H., Chakrabarti, D., Winzeler, E. A. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.08.730986</dc:identifier>
<dc:title><![CDATA[Duplication of superoxide dismutase and a mutation in aquaglyceroporin mediates the sensitivity of Plasmodium falciparum to cryptosporin, a natural product derived from Acaromyces ingoldii]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.10.731306v1?rss=1">
<title>
<![CDATA[
Evaluating anonymized genome re-identification using polygenic predictions and its implications for data privacy 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.10.731306v1?rss=1
</link>
<description><![CDATA[
Re-identification by phenotypic prediction aims to determine whether a genome belongs to a specific individual by comparing the individual's known traits with those predicted from the genome. This type of tracing attack is widely discussed in the genomic privacy literature, yet previous studies have been criticized for overstating its practical risks. Over the past decade, genome-wide association studies (GWAS) with increasing sample size improved the accuracy of phenotypic prediction, potentially enhancing such attacks. To quantify their real-world threat, we developed a probabilistic framework that estimates the likelihood of a match between an individual's observed traits and polygenic scores (PGS) derived from a genome, while accounting for prediction accuracy and genetic and environmental correlations between the traits. We benchmarked this re-identification method and examined how the prior probability (reflecting the a priori chance that a random genome and set of traits correspond to the same person) affects performance. Finally, we assessed whether sensitive information could be inferred through this attack by attempting to predict multiple sensitive haplotypes, such as APOE-{epsilon}4 (linked with Alzheimer's disease). Our re-identification method outperformed a state-of-the-art tool, and reached a precision above 99% for a recall of 40% when considering a prior of 50%. However, after considering real-world settings, we estimated that realistic priors would not exceed 4 x 10-4%, resulting in a precision lower than 0.13% at the same recall (40%). The inference of sensitive genotypes also proved ineffective, as achieving a precision above 50% for identifying APOE-{epsilon}4 carriers was only possible at a recall below 20%. To conclude, although re-identification by phenotypic prediction is technically feasible, our findings indicate that its effectiveness in real-world conditions is limited. These results counterpoint to earlier claims of severe genomic privacy risks and offer guidance for policymakers, biobank administrators, and research participants.
]]></description>
<dc:creator><![CDATA[ Cavinato, T., Hofmeister, R. J., Kutalik, Z. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.10.731306</dc:identifier>
<dc:title><![CDATA[Evaluating anonymized genome re-identification using polygenic predictions and its implications for data privacy]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.09.730678v1?rss=1">
<title>
<![CDATA[
The Gene Version Iteration Hypothesis reveals the Y chromosome-mediated closed-loop transmission and version selection mechanism of mutated genes 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.09.730678v1?rss=1
</link>
<description><![CDATA[
The Gene Version Iteration Hypothesis (GVIH) proposes that mutant genes may originate from the Y chromosome, traverse through the X chromosome to autosomes, undergo interchromosomal transfer, and potentially return to the Y chromosome via the X chromosome. This hypothetical closed transmission loop may facilitate the storage, screening, and elimination of different versions of mutant genes. The hypothesis comprises five core propositions: (1) Mutation reservoir: The Y chromosome may serve as a specialized carrier for generating mutant genes, characterized by elevated mutation rates, reduced gene density, and accelerated evolutionary dynamics; (2) Closed-loop transmission: Mutant genes may follow a unidirectional pathway Y[-&gt;]X[-&gt;]autosomes[-&gt;]X[-&gt;]Y, forming a complete transmission circuit; (3) Coexistence of multiple versions: A single functional gene may exist in multiple versions across different chromosomes, constituting a dynamic gene version library; (4) Reproductive screening: Environmentally adaptive gene versions may persist across generations and potentially migrate to upstream chromosomes, while maladaptive versions may be eliminated; (5) Terminal elimination: Gene versions reaching the Y chromosome may undergo elimination processes, potentially preventing version monopolization and maintaining evolutionary dynamics. This hypothesis provides a novel framework for understanding adaptive evolution at the genetic level. If empirically validated, it may offer new insights into the molecular mechanisms underlying certain genetic phenomena and evolutionary processes.
]]></description>
<dc:creator><![CDATA[ Liu, Y. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.09.730678</dc:identifier>
<dc:title><![CDATA[The Gene Version Iteration Hypothesis reveals the Y chromosome-mediated closed-loop transmission and version selection mechanism of mutated genes]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.09.729629v1?rss=1">
<title>
<![CDATA[
Bone response to intermittent parathyroid hormone (PTH) is both genetic and sex specific 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.09.729629v1?rss=1
</link>
<description><![CDATA[
Teriparatide (PTH 1-34) is an anabolic agent used to treat osteoporosis, yet clinical response varies widely among patients. To investigate genetic and sex-specific determinants of skeletal response, we administered intermittent PTH to male and female mice from eight genetically diverse inbred strains. Mice were treated for four weeks, and bone phenotypes were assessed via DXA, microCT, and mechanical testing. Response to PTH was highly strain- and sex-dependent, with some strains responding at the femur but not the spine, and vice versa. Heritability estimates for PTH-induced changes in bone mineral density (BMD), cortical area, breaking strength, and trabecular bone volume fraction (BV/TV) ranged from moderate to high, with BV/TV showing the strongest genetic influence. Cortical bone response mechanisms differed by sex: males exhibited periosteal expansion, while females showed endosteal remodeling. These findings mirror clinical observations where hip non-response is more prevalent than spine non-response and suggest that genetic background and sex significantly influence therapeutic outcomes. Our data support the use of genetically diverse mouse models to elucidate the genetic architecture of PTH response and highlight the potential for personalized approaches in osteoporosis treatment. Future genome-wide association studies in outbred mice may identify specific loci mediating skeletal responsiveness to PTH, advancing precision medicine strategies for bone anabolic therapies.
]]></description>
<dc:creator><![CDATA[ Adams, D. J., Godfrey, D. A., Ridoux, S., Maynard, R. D., Szeto, N. S., Ackert-Bicknell, C. L. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.09.729629</dc:identifier>
<dc:title><![CDATA[Bone response to intermittent parathyroid hormone (PTH) is both genetic and sex specific]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.07.730721v1?rss=1">
<title>
<![CDATA[
eQTM (expression quantitative trait methylation) Atlas: a comprehensive resource of over 11 million DNA methylation-gene expression associations through across 11 tissues and 4 diseases 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.07.730721v1?rss=1
</link>
<description><![CDATA[
Motivation: Epigenome-wide association studies (EWAS) have identified numerous DNA methylation (DNAm) CpG sites associated with complex traits and diseases, but interpretation of those CpG sites remains challenging because in EWAS, CpGs are mostly linked to nearby genes based only on genomic proximity. Expression quantitative trait methylation (eQTM) analyses connect DNAm CpGs with statistically associated gene expression levels. However, a comprehensive, searchable resource integrating eQTMs across diverse tissues and disease contexts has been lacking. Results: We developed the eQTM Atlas, a web-based resource that manually curates more than 11 million DNAm-gene expression associations from eight cohorts, covering 11 tissue types, four broad disease contexts, 173,886 unique CpG probes and 20,231 unique genes. The Atlas supports gene- or CpG- searches by tissue or disease type and finding associated CpG or genes, visualization of cis- and trans-eQTMs through genome browser, heatmap interfaces across various tissues, and cohort-level data downloads. By integrating eQTM results with EWAS resources, the eQTM Atlas enables users to connect disease- or trait-associated CpGs to statistically associated genes rather than relying solely on proximity-based gene annotation, supporting functional interpretation of EWAS findings and generation of disease-specific regulatory hypotheses. Availability and implementation: The eQTM Atlas is freely available at https://shiny.crc.pitt.edu/eqtm_browser/. The web interface is implemented in R Shiny and hosted through the University of Pittsburgh Center for Research Computing (CRC). Source code is available at https://github.com/ads303/eQTM-Atlas.
]]></description>
<dc:creator><![CDATA[ Sriram, A., Kim, S., Caldino Bohn, R., Chen, W., Liu, T., Yue, M., Jain, N., Pierce, B., Joehanes, R., Levy, D., Patin, E., Quintana-Murci, L., Park, H. J., Celedon, J. C. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.07.730721</dc:identifier>
<dc:title><![CDATA[eQTM (expression quantitative trait methylation) Atlas: a comprehensive resource of over 11 million DNA methylation-gene expression associations through across 11 tissues and 4 diseases]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.07.724338v1?rss=1">
<title>
<![CDATA[
Buried in two places: Lineages from elite Maya tombs also found in distant caves 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.07.724338v1?rss=1
</link>
<description><![CDATA[
Classic Period Maya societies 250-900 CE carved out urban centers from the rainforest reaching population heights and political complexity previously unknown in the Mesoamerican tropics. Kinship was a central feature of the social fabric, and rulership was legitimized through claims of direct descent from mythical ancestors. Mortuary practices kept the dead close to the living, and ancestor veneration sometimes produced complex deposits of disarticulated remains that are difficult to identify and whose relationship to each other cannot be understood without genetic data. We screened 487 samples and successfully generated genome-wide data for 430 samples from at least 145 distinct individuals from an Early Classic Period kingdom 250-750 CE in the rugged Maya Mountains of Belize. Of these, 24 individuals have body parts in both an elite tomb, and in a ritual tooth cache in a distant cave on the other side of the Maya mountains. These results show elite lineages created ancestors from their deceased relatives in geographically expansive ways and highlights the importance of caves in the belief system of Classic Maya elites.
]]></description>
<dc:creator><![CDATA[ Brielle, E. S., Dorgay, E., Kennett, D. J., Mes, J., Moes, E., Neff, N. C., Novotny, A. C., Rangel, E., Ray, E. E., Robinson, M., Thompson, A. E., Warner, M., Akbari, A., Callan, K., Caughran, E., Fournier, R., Frost, T., Iliev, L., Kearns, A., Kellogg, J., Lawson, A. M., Lazaridis, I., Mah, M., Manjila, N., Nawaz, M., Olalde, I., Oppenheimer, J., Patterson, I., Qiu, L., Sirak, K., Soos, G., Workman, J. N., Mallick, S., Rohland, N., Reich, D., Prufer, K. M. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.07.724338</dc:identifier>
<dc:title><![CDATA[Buried in two places: Lineages from elite Maya tombs also found in distant caves]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.08.730819v1?rss=1">
<title>
<![CDATA[
Tracking kdr Alleles Associated with Pyrethroid Resistance in Aedes albopictus across Italy: A Nationwide Genotypic Dataset by MosqIRIT Network. 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.08.730819v1?rss=1
</link>
<description><![CDATA[
This data paper presents a curated, georeferenced dataset of the frequencies of the two main target site mutations (V1016G and F1534C) associated with resistance to pyrethroid insecticides in Aedes albopictus in Italy. Populations were collected in 102 out 107 Italian provinces between 2023 and 2025. Specimens were sampled by members of the Mosquito Insecticide Resistance Italian Network (MosqIRIT) as part of RN2 activities within the INF-ACT project. Genotyping was performed on 3,517 individuals by specific allele-specific PCR assays. Each record includes metadata on sampling site, administrative location, developmental stage, collection method, and mutation-specific genotype frequencies. To support spatial analysis modelling effort, the dataset integrates geographic, eco-climatic, and demographic data. This resource will support mosquito control programs, pyrethroid resistance monitoring and managing, as well as ecological modelling, and is compliant with the FAIR data program.
]]></description>
<dc:creator><![CDATA[ De Marco, C. M., Pichler, V., Gobbo, F., Manzi, S., Rosso, E., Toniolo, F., Carra, E. M., Petrella, A., Grisendi, A., Defilippo, F., Tessarolo, C., Ercole, E., Accorsi, A., Mosca, A., Cassina, F., di domenico, M., Di Lollo, V., De Ascentis, M., D'Alessio, S. G., Congiu, i., Donati, V., Carioti, V., Badieinia, F., Gavaudan, S., Canonico, C., Favia, G., Racciatti, F., Spaccapelo, R., Alami, C., De Martinis, C., Pucciarelli, A., Picazio, G., Viscardi, M., Capozzi, L., Cariglia, M. G., Violante, L., Foxi, C., Dedola, D., Sini, V., Ruiu, L., Vinci, A., Scibetta, S., Oliveri, E., Reale, S., Di Pasqu ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.08.730819</dc:identifier>
<dc:title><![CDATA[Tracking kdr Alleles Associated with Pyrethroid Resistance in Aedes albopictus across Italy: A Nationwide Genotypic Dataset by MosqIRIT Network.]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.06.730570v1?rss=1">
<title>
<![CDATA[
Use of a plasmid containing a dual gene reporter system to assess the cell hydrophobicity of Listeria monocytogenes 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.06.730570v1?rss=1
</link>
<description><![CDATA[
Listeria monocytogenes causes listeriosis in humans and animals and contaminates prepared food by attaching to food processing environments. Therefore, closer monitoring of how the organism adheres to surfaces will help identify ways to prevent it from colonising food-processing environments. To develop new attachment assays, clinical and environmental strains of L. monocytogenes were transformed by inserting a plasmid containing lux, gfp reporter genes and an erythromycin-resistant gene into the parent cells. Transformed cells were grown for 48 hours on brain heart infusion agar plates containing erythromycin, after which the cells were viewed under a molecular light imager and luminometer. Fluorescent cells containing the gfp, lux, and erythromycin-resistant genes were visible, whereas control cells without the plasmid were not. Transformation efficiency was highest with the environmental strains, and subsequent growth and hydrophobicity tests carried out with the transformed cells in different growth conditions showed that they were able to attach well to solvents when compared to the parent cells. However, the growth rate of the transformed cells was poor, indicating a disruption of cell metabolism. Results show the possibility of real-time monitoring of how cells attach to different surfaces and could lead to a better understanding of the initial colonisation of a surface by the organism.
]]></description>
<dc:creator><![CDATA[ Nwaiwu, O., Rees, C. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.06.730570</dc:identifier>
<dc:title><![CDATA[Use of a plasmid containing a dual gene reporter system to assess the cell hydrophobicity of Listeria monocytogenes]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.05.730474v1?rss=1">
<title>
<![CDATA[
Outbred Drosophila populations reveal diet-dependent genetic effects on development time 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.05.730474v1?rss=1
</link>
<description><![CDATA[
Metabolic effects of genetic variation often depend on diet, yet the loci underlying diet-dependent developmental responses remain incompletely defined. Here we combine multi-trait phenotyping of Drosophila Genetic Reference Panel lines with genome-wide mapping in newly developed Drosophila Recombinant Populations. High sugar causes genotype- and life-stage-dependent changes in metabolic and life-history traits, with development time emerging as a highly heritable, sugar-sensitive phenotype. Mapping in 16 outbred advanced intercross populations reveals distinct association landscapes under low- and high-sugar diets, with a concentrated low-sugar signal, a more distributed high-sugar pattern, and identified genotype-by-diet loci including tap, Eip75B and Cerk. Functional perturbation supports diet-dependent effects for several prioritized candidates. Allele-frequency analyses identify operationally defined thrifty-like variants associated with delayed development under high sugar and relatively earlier development under low sugar; these variants are enriched for cell-adhesion, neurodevelopmental, and morphogenetic processes. Together, these results establish an outbred Drosophila framework for dissecting how dietary sugar remodels the genetic architecture of development time.
]]></description>
<dc:creator><![CDATA[ Bai, Y., Shabbir, S., Chen, Y., Morgante, F., Ludwig, M., Park, S.-Y., Acharya, M., Li, Y., Ali, S., Trudnak, A., Rajesh, M., Kreitman, M., Zhuang, X. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.05.730474</dc:identifier>
<dc:title><![CDATA[Outbred Drosophila populations reveal diet-dependent genetic effects on development time]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.06.730627v1?rss=1">
<title>
<![CDATA[
Multi-Trait Meta-QTL Analysis Reveals Genomic Hotspot Classes for Strategic Maize Improvement 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.06.730627v1?rss=1
</link>
<description><![CDATA[
Abstract Background Decades of maize (Zea mays L.) QTL mapping have produced fragmented results across hundreds of independent studies, characterized by broad confidence intervals, population-specific effects, and a predominantly single-trait analytical scope. Comprehensive multi-trait integration remains limited, yet it could substantially improve our understanding of trait relationships for strategic breeding. We integrated 2,701 QTLs published over 30 years across five functionally distinct trait categories (grain yield and components; plant development and architecture; plant physiology and stress adaptation; grain quality and nutritional composition; and disease and pest resistance) in order to identify functionally classified genomic hotspots and prioritize candidate genes for multi-trait breeding applications. Results BioMercator V4.2 consolidated 2,518 projectable QTLs into 187 high-confidence meta-QTLs (MQTLs), achieving an average 59% reduction in confidence interval width; 128 of 187 MQTLs (68.4%) achieved dual-platform support through GWAS co-localization. Twenty-three genomic hotspots harbored 132 of 187 MQTLs (70.6%) and were classified into three functional categories: twelve multi-trait hubs that may enable simultaneous improvement of multiple traits through pleiotropic or tightly linked genes; seven single-trait clusters with pathway-specific effects, exemplified by the chromosome 9 starch biosynthesis cluster; and four major-effect loci with reported individual effects exceeding 20% PVE, including vgt1 (54% PVE) and opaque2 (34.2% PVE). Descriptive environmental classification distinguished MQTLs predominantly supported by optimal-condition QTLs (42%) from those predominantly supported by stress-condition QTLs (28%), the latter showing approximately 3.5-fold greater mean contributing-QTL phenotypic variance, directionally consistent with conditional genetic effect amplification under stress. Network-based candidate gene prioritization combined with cross-cereal ortholog analysis showed that 67% of the top candidates possess orthologs in rice, sorghum, wheat, or barley, and 53% are conserved across all four species, identifying priority targets for functional genomics investment. Conclusions This functionally classified and environmentally characterized meta-QTL framework provides breeders with a structured resource for multi-trait hotspot selection, environment-appropriate allele deployment, and functional genomics prioritization, with broader applicability as a transferable analytical template for other crop species confronting analogous challenges of fragmented QTL literature and complex multi-trait breeding objectives.
]]></description>
<dc:creator><![CDATA[ Parthasarathy, S., Rocheford, T., Koehler, K. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.06.730627</dc:identifier>
<dc:title><![CDATA[Multi-Trait Meta-QTL Analysis Reveals Genomic Hotspot Classes for Strategic Maize Improvement]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.07.730749v1?rss=1">
<title>
<![CDATA[
Genomic instability within a sympatric complex of South American garlics (Nothoscordum spp., Amaryllidaceae) 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.07.730749v1?rss=1
</link>
<description><![CDATA[
Background and Aims: The evolution of reproductive isolation between previously interbreeding populations is a fundamental driver of plant speciation. Within Amaryllidaceae, Nothoscordum represents an evolutionarily complex genus, characterized by an unusually high incidence of chromosomal rearrangements. During fieldwork, Nothoscordum montevidense and Nothoscordum bonariense were found growing in sympatry, along with individuals exhibiting intermediate morphological traits, suggesting a putative hybrid origin. To test this hypothesis, we employed an integrative approach to characterize the morphologically intermediate specimens and the two sympatric populations. Materials and methods: To characterize the putative hybrids we have combined morphological, cytogenetic analyses (chromosome counts, CMA/DAPI banding, and FISH) and flow cytometry-based genome size estimation. Phylogenetic relationships and genomic structure were also investigated through Genotyping-by-Sequencing (GBS), complete chloroplast genome assembly, and comparative repetitive DNA analysis. We also performed species distribution modeling and phenological analyses of the putative parental species. Key Results: Multiple lines of evidence confirm the hybrid origin of the studied plants. Cytogenetic analyses revealed specimens with 2n = 21 (1C {approx} 33 pg = 32.274 Mbp) and 2n = 25 (1C {approx} 37 pg = 36.186 Mbp), accompanied by meiotic irregularities consistent with interspecific hybridization. Chloroplast genome phylogeny identified N. montevidense (2n = 16, 1C {approx} 25 pg) as the maternal lineage, while GBS data confirmed N. bonariense (2n = 26, 1C {approx} 41 pg) as the paternal contributor and revealed evidence of subsequent backcrossing. Comparative analysis of repetitive DNA showed reduced 35S rDNA diversity in the hybrid, indicative of post-hybridization genomic restructuring. Despite the observed genomic complexity, no clear morphological differentiation was detected among hybrid individuals. Phenological analyses and species distribution models demonstrated broad overlap between parental species. Conclusions: Our findings highlight the role of hybridization in shaping genome architecture in cytogenetically labile plant lineages. Furthermore, our results underscore that morphological similarity can mask profound genomic complexity, reinforcing the value of integrative approaches to understand genera characterized by reticulate evolution and genomic instability.
]]></description>
<dc:creator><![CDATA[ Sassone, A. B., Sader, M. A., Nascimiento, T. E., Blattner, F. R., Giussani, L. M. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.07.730749</dc:identifier>
<dc:title><![CDATA[Genomic instability within a sympatric complex of South American garlics (Nothoscordum spp., Amaryllidaceae)]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.09.731113v1?rss=1">
<title>
<![CDATA[
Research Process Graph: LLM-Driven Extraction and Hierarchical Organization of Research Logic 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.09.731113v1?rss=1
</link>
<description><![CDATA[
Plant biology now publishes thousands of experimental research articles each year, but their core research logic, namely what questions are being asked, with what methods, and what is being found, remains locked inside free text and invisible to systematic analysis. Here we present a structured, 20-year atlas of The Plant Cell in which every paper is converted into a typed, directed Research Process Graph (RPG) of Question (Q), Method (M) and Finding (F) nodes connected by Q[-&gt;]M and M[-&gt;]F edges. A benchmarked large language model pipeline applied to 2,633 Plant Cell research articles published 2005-2026 recovered >110,000 Q/M/F nodes and >126,000 directed Q[-&gt;]M[-&gt;]F chains with>98% precision. A second LLM pass generalises each node into a paper-independent canonical form and assigns it to one of 10 top-level (L1) and ~90 sub-level (L2) categories for each node type, producing the first comprehensive map of plant-biology research logic at the resolution of individual research questions. The atlas reveals that Plant Cell papers fall into seven canonical paper recipes with characteristic Q[-&gt;]M[-&gt;]F sub-structures, that peripheral experimental techniques have largely turned over while a stable methodological core persisted, and that the strongest correlate of per-PI citation impact is methodological breadth, not productivity or topical breadth. We release the atlas as a public, browsable database with five complementary interfaces: paper views, an LLM-powered research assistant, expert profiles, a taxonomy browser, and a method explorer. The database, available at https://rpg.connectome.tools/, turns the literature into a queryable community resource.
]]></description>
<dc:creator><![CDATA[ Yang, J., Itharajula, M., Mutwil, M. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.09.731113</dc:identifier>
<dc:title><![CDATA[Research Process Graph: LLM-Driven Extraction and Hierarchical Organization of Research Logic]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.09.731038v1?rss=1">
<title>
<![CDATA[
Hydroxylated monoterpenes mimic bacterial attack to trigger jasmonate-dependent self-amplifying immunity in tomato 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.09.731038v1?rss=1
</link>
<description><![CDATA[
Hydroxylated monoterpenes (HMTPs) are emitted during resistant tomato-Pseudomonas syringae interactions and confer antibacterial resistance, yet their integration into immune signalling remains poorly understood. Here we show that HMTPs act as endogenous mimics of pathogen attack that engage canonical defence pathways in tomato. Using -terpineol as a representative HMTP, we demonstrate that this volatile activates MPK kinase-, calcium- and reactive oxygen species (ROS)-dependent signalling, promotes jasmonate and salicylic acid accumulation, and induces pathogen-like stomatal immunity independently of abscisic acid. Functional analyses revealed that HMTPs biosynthesis depends on ROS and jasmonate signalling, and HMTPs further promote their own accumulation, establishing a self-reinforcing feed-forward mechanism. Moreover, in vitro oxidative conditions drive chemical remodelling and selective interconversion among HMTPs, contributing to volatile diversification and favouring the accumulation of highly bioactive hydroxylated forms. Consistently, deuterium-labelled linalool is incorporated into plant metabolism and converted into deuterated -terpineol in planta, providing direct evidence for volatile interconversion. Together, our findings establish HMTPs as dynamic amplifiers of tomato antibacterial immunity and key actors in pathogen-associated signalling.
]]></description>
<dc:creator><![CDATA[ Perez-Perez, J., Brito-Gutierrez, P., Santiago, A., Sanmartin, M., Matus, T., Sulli, M., Diretto, G., Vera-Sirera, F., Rodrigo, I., Lopez-Gresa, M. P., Lison, P. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.09.731038</dc:identifier>
<dc:title><![CDATA[Hydroxylated monoterpenes mimic bacterial attack to trigger jasmonate-dependent self-amplifying immunity in tomato]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.10.731257v1?rss=1">
<title>
<![CDATA[
Cf-4- and Cf-5-triggered plant immunity: Similarities and differences 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.10.731257v1?rss=1
</link>
<description><![CDATA[
Abstract Plant immunity is, amongst others, mediated by receptor like proteins (RLPs), which are localized on the plasma membrane. RLPs recognize extracellular immunogenic patterns (ExIPs) originating from pathogens or derived from the host itself, which leads to extracellularly triggered immunity (ExTI). Cf proteins, which are well-known RLPs of tomato (Solanum lycopersicum) confer resistance against the fungal pathogen Fulvia fulva. Cf-9, Cf-4, Cf-2 and Cf-5 are well-known examples of Cf proteins, mediating recognition of the matching ExIPs Avr9, Avr4, Avr2 and Avr5, respectively, which are secreted effectors of F. fulva and trigger hypersensitive response (HR)-related cell death in tomato plants carrying these Cf proteins. Although all these Cf proteins confer proper resistance to the fungus, Cf-9 and Cf-4 trigger a stronger and faster cell death than Cf-5 and Cf-2. It is unknown whether these phenotypical differences arise from variations in the molecular mechanism of the cellular immune response that is initiated by the Cf proteins, and whether this phenotypic difference correlates with varying degrees in the intensity and timing of the triggered immune responses and robustness of the resistance. To try to answer these questions, in this study the immune responses triggered by Cf-4 and Cf-5 were compared. Cf-4 and Cf-5 share the same core upstream signaling components to trigger HR-related cell death in Nicotiana benthamiana. In tomato, both receptors induce rapid MAPK activation, which is more sustained for the Cf-5/Avr5 combination. Both Avr4 and Avr5 induce an apoplastic burst of reactive oxygen species (ROS), independently of the presence of their matching receptors, while remaining dependent on RBOHB for this ROS burst. Full transcriptome analysis at 3 and 7 hours after immune activation revealed a large shared set of differentially expressed genes, alongside qualitative and quantitative differences, with the Cf-5/Avr5 combination inducing a broader transcriptional reprogramming. Despite these differences, Cf-4 and Cf-5 confer a comparable level of resistance to F. fulva. These results demonstrate that Cf-4 and Cf-5 share conserved immune initiation mechanisms, but diverge in downstream signaling dynamics, and that the intensity and timing of the HR-related cell death do not affect the robustness of the resistance.
]]></description>
<dc:creator><![CDATA[ Budak, E., Aguiar Canha, H., Joosten, M. H. A. J. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.10.731257</dc:identifier>
<dc:title><![CDATA[Cf-4- and Cf-5-triggered plant immunity: Similarities and differences]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.08.730374v1?rss=1">
<title>
<![CDATA[
Higher Lipid Saturation in Well-Irrigated Georgia Cotton Plants: A Field-Based NMR Metabolomics Study 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.08.730374v1?rss=1
</link>
<description><![CDATA[
Cotton (Gossypium hirsutum) is an economically important crop, but it faces increasing pest outbreaks, especially in non-irrigated areas. In this study, 20 cotton farms using center-pivot irrigation were sampled in southern Georgia to assess chemical differences between non-irrigated and irrigated areas. Proton (1H) nuclear magnetic resonance (NMR) data were obtained from cotton leaves, and Principal Component Analysis (PCA) was performed to assess differences in chemical composition. Across all samples, farm site accounted for most of the variability, but within each farm site, the PCA scores plots showed clear separation between non-irrigated and irrigated conditions in 10 sites. Inspecting the PCA loadings revealed significant resonances resembling a lipid-like signal. After reverse-phase fractionation, we observed that many of these resonances appeared together in later fractions, suggesting a lipid, specifically a fatty acid such as linoleic acid. We hypothesized that differences in net lipid saturation level may drive separation between non-irrigated and irrigated samples. Six farm sites had a significantly or marginally significantly higher degree of unsaturation in irrigated samples, while one farm site had significantly higher unsaturation in non-irrigated samples. Our results indicate that drought stress likely affects lipid profile composition, which could be driving higher herbivorous pest densities in drought-stressed crops.
]]></description>
<dc:creator><![CDATA[ Patel, K., Esselman, C. S., Croy, J., Gillis, M., Rodrigues, P. A. P., Simmons, A., Borges, R. M., Edison, A. S., Snyder, W. E. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.08.730374</dc:identifier>
<dc:title><![CDATA[Higher Lipid Saturation in Well-Irrigated Georgia Cotton Plants: A Field-Based NMR Metabolomics Study]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.08.730953v1?rss=1">
<title>
<![CDATA[
The plant immune receptor LORE binds agonistic and antagonistic 3-hydroxy fatty acid ligands via a dynamic loop in its G-type lectin domain 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.08.730953v1?rss=1
</link>
<description><![CDATA[
The Arabidopsis thaliana S-domain receptor kinase LORE senses bacterial medium-chain 3-hydroxy fatty acids (mc-3-OH-FAs) as microbe-associated molecular patterns to activate pattern-triggered immunity. How LORE recognises these fatty acid ligands at the molecular level remains unknown. Here, we combined protein structure prediction, protein-ligand interaction modelling and molecular dynamics (MD) simulations with ligand-binding assays using chimeric and mutant receptor ectodomains, and functional analysis of receptor activation to characterise the mc-3-OH-FA binding mechanism. Domain-swap experiments between LORE and its non-binding paralog AtSD1-23 identify the lectin 2 (L2) domain as the ligand-binding domain. Mutational analysis and reverse engineering confirm a hydrophobic pocket in the L2 core as the primary ligand-binding site. Multiple walker Supervised MD (mwSuMD) simulations reveal that the acyl tail enters the pocket first, whilst polar interactions between the headgroup and a flexible L2 loop guide and stabilise the bound state. In support of this model, 3-OH-C10:0 analogues with bulky headgroup modifications dock into the pocket but act as antagonists, presumably by preventing the loop from adopting the conformation required for signalling. Together, these data suggest that the flexible L2 loop has multiple functions: it acts as a dynamic gate regulating pocket access, provides essential anchoring points once the ligand is bound, and contributes to receptor activation. These findings provide a mechanistic framework for immunogenic mc-3-OH-FA sensing by LORE.
]]></description>
<dc:creator><![CDATA[ Shu, L.-J., Nicoli, A., Yu, F.-Y., Thiry, O. O. A., Deslandes-Herold, G., Luethi, T., Di Pizio, A., Ranf, S. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.08.730953</dc:identifier>
<dc:title><![CDATA[The plant immune receptor LORE binds agonistic and antagonistic 3-hydroxy fatty acid ligands via a dynamic loop in its G-type lectin domain]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.08.730856v1?rss=1">
<title>
<![CDATA[
Dual Knockout of StAMY23 and StVINV Improves Postharvest Storage Traits in Potato 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.08.730856v1?rss=1
</link>
<description><![CDATA[
Starch is the primary carbohydrate reserve in potato (Solanum tuberosum L.) tubers and a critical determinant of their industrial value. The rate of starch degradation during postharvest storage directly influences key traits such as endodormancy (ED) duration and cold-induced sweetening (CIS), which affect sprouting behavior. In this study, we used CRISPR/Cas9 genome editing to knockout StAMY23, a gene encoding -amylase involved in starch breakdown. stamy23 plants exhibited higher yield and extended tuber ED postharvest, without significantly altering CIS or starch granule content. To further reduce CIS, we knockout StAMY23 in VACUOLAR INVERTASE knockout (stvinv) backgrounds, generating stamy23/stvinv double-knockouts plants. These lines showed significantly reduced CIS, prolonged ED, and elevated starch content, along with altered starch granule content. Collectively, our findings demonstrate that simultaneous downregulation of StAMY23 and StVINV can additively enhance desirable postharvest traits, providing a promising strategy for improving potato storage quality through precision genome editing.
]]></description>
<dc:creator><![CDATA[ Teper-Bamnolker, P., Steinberg, T., Shtein, C., Peer, R., Doron-Faigenboim, A., Belausov, E., Sherman, A., Eshel, D. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.08.730856</dc:identifier>
<dc:title><![CDATA[Dual Knockout of StAMY23 and StVINV Improves Postharvest Storage Traits in Potato]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.08.730999v1?rss=1">
<title>
<![CDATA[
Rational design of T-DNA vectors enables predictable, single-copy integration in Arabidopsis thaliana 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.08.730999v1?rss=1
</link>
<description><![CDATA[
Agrobacterium-mediated transformation is the dominant method for plant transgenesis, yet it frequently produces multi-copy, structurally complex T-DNA insertions associated with transgene silencing, unpredictable expression, and genome instability. Here, leveraging a high-throughput phenotypic reporter, we systematically dissect how T-DNA vector architecture, plasmid biology, and regulatory element choice shape transformation outcomes in Arabidopsis thaliana. We discover a pronounced trade-off between transformation efficiency and T-DNA copy number, uncovering the virulence enhancing overdrive sequence as a major determinant of this relationship. Guided by these insights, we engineered a new T-DNA vector that balances efficient transformation with predominantly single-copy integration. Additionally, we replaced viral elements, such as the widely used CaMV 35S promoter, with Arabidopsis-derived regulatory elements to minimise undesired enhancer effects, and developed a streamlined workflow for efficient T-DNA insertion mapping in the genome. Together, these advances form the T1 vector series, an Arabidopsis-optimised T-DNA vector system that enables clean, single-copy, and readily mappable transgene integration with predictable expression in the first generation after transformation.
]]></description>
<dc:creator><![CDATA[ Shaw, W. M., Gajendiran, A., Tchantouridze, E. I., Bechen, L. L., Clarke, S. G., Guiziou, S., Gehring, M., Khalil, A. S. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.08.730999</dc:identifier>
<dc:title><![CDATA[Rational design of T-DNA vectors enables predictable, single-copy integration in Arabidopsis thaliana]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.06.730605v1?rss=1">
<title>
<![CDATA[
The coordination between xylem and bark hydraulics in temperate Rosaceae species 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.06.730605v1?rss=1
</link>
<description><![CDATA[
Xylem and bark properties influence tree growth and drought resistance, yet their functional coordination and their environmental drivers remain unclear. We assessed xylem-bark coordination in branches of eight temperate woody Rosaceae species spanning different ecological preferences. We quantified xylem hydraulic efficiency and safety alongside bark traits governing permeability, hygroscopic water exchange, water storage, and anatomy, and evaluated phylogenetic signal and climatic associations. Bark water vapor conductance (Gbark) increased with maximum xylem hydraulic conductivity (Kh) and with xylem water potential at 50% loss of conductivity (P50), indicating species with more efficient but more embolism-vulnerable xylem developed more permeable bark. Species with higher Gbark showed reduced hygroscopic absorption time, consistent with faster rehydration from atmospheric water vapor. Both Gbark and P50 were phylogenetically conserved and covaried with climatic factors, namely air temperature, vapor pressure deficit (VPD), and isothermality. Species from warmer, high-VPD climates with greater diurnal temperature variability combined higher bark permeability with more vulnerable xylem, implying a shift from embolism avoidance to embolism tolerance strategies. Overall, xylem and bark hydraulics in Rosaceae evolved in concert along diurnal and annual gradients of evaporative demand, showing that drought resistance in woody angiosperms cannot be understood without considering bark traits alongside xylem function.
]]></description>
<dc:creator><![CDATA[ Jupa, R., Patkova, T., Binter, J., Dolezal, J., Nobis, M. P., Mayr, S., Gloser, V. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.06.730605</dc:identifier>
<dc:title><![CDATA[The coordination between xylem and bark hydraulics in temperate Rosaceae species]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.07.730737v1?rss=1">
<title>
<![CDATA[
Evaluating crop models for future climate scenarios: wheat yield predictions using APSIM and STICS under combined CO2, warming, and water deficit conditions 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.07.730737v1?rss=1
</link>
<description><![CDATA[
Crop models are essential for predicting climate change impacts on agriculture, yet their validation under multi-stress conditions remains limited. This study evaluated two widely-used wheat models, APSIM and STICS, using data from three Free-Air CO2 Enrichment (FACE) experiments (USA, Germany, Australia) combining elevated CO2 (eCO2), water deficit, and warming. Environmental characterisation using simulation-based stress indices revealed that intended "controls" frequently experienced hidden heat and water stress, meaning models were calibrated on crops already undergoing physiological adjustments. Evaluation of simulated yield and components revealed a clear hierarchy in prediction errors (RRMSE): unlimited conditions (3-9%) < single stress (4-27%, with a need to improve response to heat stress) < combined stress (17-123%). Elevated CO2 generally increased prediction uncertainty for crops experiencing water stress. Our results suggest that current stress functions from the models fail to capture the synergistic coupling between drought and heat stress. This highlights the urgent need for more mechanistic modelling to improve the reliability of climate change impact assessments.
]]></description>
<dc:creator><![CDATA[ Severini, A. D., Gawinowski, M., Bancal, M.-O., Launay, M., Deswarte, J.-C., Chenu, K. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.07.730737</dc:identifier>
<dc:title><![CDATA[Evaluating crop models for future climate scenarios: wheat yield predictions using APSIM and STICS under combined CO2, warming, and water deficit conditions]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.06.09.731087v1?rss=1">
<title>
<![CDATA[
Immunoengineered Chitosanase-Produced Chitosan Oligomers for Elevating Plant Resistance to Viral Infection 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.06.09.731087v1?rss=1
</link>
<description><![CDATA[
Chitooligomers can act as plant biostimulants or biopesticides, but current chitosan-based agro-biologics often lack sufficient efficacy. This is due to a lack of scalable production processes for structurally well-controlled chitosans combined with a limited understanding of structure-function relationships. Chitosans differ in their degree of polymerization (DP), fraction and pattern of acetylation (FA and PA). While the influence of DP and FA on antimicrobial and phytostimulatory properties is at least partially known, this is not yet the case for PA. PA can be partially controlled by using enzymatic rather than acid hydrolysis for oligomer production. We have used recombinant chitinases and chitosanases to hydrolyse a well-characterised chitosan polymer, and purified oligomers with different DP. We have structurally characterised the products and tested their abilities to protect tobacco from viral disease. Chitinase products were dominated by GlcNAc units at their reducing and non-reducing ends, with GlcN units dominating their centers, and v.v. for chitosanase products. While the chitinase-derived hydrolysates were inactive, the chitosanase-derived oligomers possessed elicitor and priming activities and protected plants from disease, and their activity increased with increasing DP. Clearly, the Bacillus chitosanase used is well-suited to set up a scalable production process for chitosan oligomers with promising agro-biologic properties.
]]></description>
<dc:creator><![CDATA[ Khanahmadi, S., Singh, R., Ryll, J., Nava Cruz, N. Y., Cord-Landwehr, S., Richter, C., Rafieerad, A., Moerschbacher, B. M. ]]></dc:creator>
<dc:date>2026-06-10</dc:date>
<dc:identifier>doi:10.64898/2026.06.09.731087</dc:identifier>
<dc:title><![CDATA[Immunoengineered Chitosanase-Produced Chitosan Oligomers for Elevating Plant Resistance to Viral Infection]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-06-10</prism:publicationDate>
<prism:section></prism:section>
</item>
</rdf:RDF>
