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<title>bioRxiv Subject Collection: Genetics Plant Biology</title>
<link>https://biorxiv.org</link>
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This feed contains articles for bioRxiv Subject Collection "Genetics Plant Biology"
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<link>https://www.biorxiv.org</link>
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<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.04.749444v1?rss=1">
<title>
<![CDATA[
Activity-level evaluation of DNA transfer to stockings: comparisonof HaloGen with simplified contributor-based approaches 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.04.749444v1?rss=1
</link>
<description><![CDATA[
DNA findings on clothing are often evaluated at sub-source level to address whether a person contributed DNA to a sample. In many cases, however, the disputed issue is not whose DNA is present, but how the DNA was transferred. This paper applies the HaloGen framework to evaluate DNA findings on stockings under activity-level propositions. The data derive from controlled experiments, reported in a companion paper, comparing active contact, in which a person of interest pulled down a pair of stockings, with social contact, in which the person of interest and wearer used the same bathroom. Contributor-specific DNA quantities were estimated for the person of interest and for observed unknown contributors across two sampled stains. Compatibility diagnostics indicated that the stockings dataset was broadly compatible with the observed Pop20 reference range. Pop20 was therefore used as regularising prior information in the Lab-Bayes model, rather than as a stand-alone Group model. Because the stockings dataset was generated in a single laboratory, transfer data from 20 laboratories were used as regularising prior information for a laboratory-specific Lab-Bayes model. The local stockings data then updated the direct- and secondary-transfer parameter distributions. Compatibility diagnostics indicated that the stockings dataset was broadly compatible with the observed Pop20 reference range. Pop20 was therefore used as regularising prior information in the Lab-Bayes model, rather than as a stand-alone Group model. In addition, prior-sensitivity and leave-one-case-out analyses indicated that the case-level likelihood ratios were not materially affected by the choice of prior specification or by data reuse. HaloGen likelihood ratios were assessed using Tippett plots and compared with simplified contributor-based comparator approaches. These approaches represent simplified forms of activity-level reasoning in which the DNA result is reduced to binary or categorical states. They comprise a binary source-support approach, a discrete Mx component-size approach, and a background approach based on the ReAct I Experiment 3 formulation. These approaches were used to examine the effect of reducing continuous contributor-specific DNA quantities to binary or categorical states, and to assess how the likelihood ratio is affected when observed unknown contributors are represented through a background/direct-unknown term rather than evaluated explicitly as possible alternative direct actors. HaloGen showed clear discrimination between active-contact and social-contact ground-truth cases. The simplified comparator methods illustrated the information loss caused by thresholding or categorising continuous DNA quantities. The ReAct background approach tended to shift direct-transfer likelihood ratios upward relative to the HaloGen calculation, showing that the treatment of observed unknown contributors can materially affect activity-level inference. The results support the importance of preserving contributor-level symmetry: an observed unknown contributor should not automatically be demoted to background when that contributor may represent an alternative direct actor under the defence proposition.
]]></description>
<dc:creator><![CDATA[ Gill, P., Johannessen, H., Borsum, C., Fonnelop, A. E., Bleka, O. ]]></dc:creator>
<dc:date>2026-09-09</dc:date>
<dc:identifier>doi:10.64898/2026.09.04.749444</dc:identifier>
<dc:title><![CDATA[Activity-level evaluation of DNA transfer to stockings: comparisonof HaloGen with simplified contributor-based approaches]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.03.749263v1?rss=1">
<title>
<![CDATA[
mRNA editing of the Alzheimer's risk gene APOE 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.03.749263v1?rss=1
</link>
<description><![CDATA[
Variants in the human APOE gene govern the risk of Alzheimer's disease and other disorders. Three major APOE variants in humans reflect C to T replacements at two positions in a single exon: an upstream variant (AE4 site) that differs between the ancestral APOE epsilon 4 allele (APOE4) (C) and human-specific APOE2/E3 (T), and a downstream variant (AE2 site) that differentiates APOE3/E4 (C) from APOE2 (T). It has long been assumed that APOE allelotypes are genomically encoded, but here we report that multiple individuals express brain APOE C or U/T variant transcripts that differ from genomically templated versions. We demonstrate up to 10% C to U, or U to C nucleotide replacement at AE4 and AE2, but not at other sites, and with no corresponding changes in genomic DNA. Single-cell transcriptomic datasets from brain microglia revealed sporadic (up to ~8%) C to U replacement at AE2. We found 0.4 to 1.6% of brain transcripts in human APOE knock-in mice harbor selective C to U changes at either AE4 or AE2 sites. Transfection of HepG2 or Huh7 cells with either mouse or human APOBEC1 led to efficient (>90%) C to U editing of APOE4 mRNA at the AE4 but not AE2 site, with lower (<10%) C to T editing of genomic DNA at the AE4 site by mouse, but not human, APOBEC1. Furthermore, interrogation of proteomic datasets revealed up to 4% of non-genomically encoded APOE peptides in human plasma, indicating that the edited APOE transcripts are functional in vivo. These data suggest that APOE mRNA is subject to RNA editing that interconverts the different allelic forms of APOE.
]]></description>
<dc:creator><![CDATA[ Blanc, V., Griffiths, S. J., Haas, J., Davidson, N., Lathe, R. ]]></dc:creator>
<dc:date>2026-09-09</dc:date>
<dc:identifier>doi:10.64898/2026.09.03.749263</dc:identifier>
<dc:title><![CDATA[mRNA editing of the Alzheimer's risk gene APOE]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.03.749262v1?rss=1">
<title>
<![CDATA[
PRDM9 Alleles Guide Distinct Patterns of Recombination Localization in Atlantic Salmon 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.03.749262v1?rss=1
</link>
<description><![CDATA[
Meiotic recombination in many vertebrate lineages is directed to genomic regions by the DNA-binding protein PRDM9. To date, PRDM9 research has focused primarily on mammals, and its role in recombination localization has only recently been established in salmonids. PRDM9 binding specificity is determined by a tandemly repeated zinc-finger array that exhibits extensive allelic diversity within and between species. However, the extent to which PRDM9 variation shapes recombination landscapes in salmonids remains poorly understood. Here, we performed large-scale genotyping of PRDM9 in an aquaculture population of Atlantic salmon (Salmo salar) using long-read sequencing. By integrating PRDM9 genotypes with pedigree information and genome-wide recombination data, we generated PRDM9-specific linkage maps and sets of inferred crossover events. We show that the presence of specific PRDM9 alleles is associated with differences in recombination localization and identify patterns consistent with dominance interactions between alleles. Using population-averaged recombination rate estimates, we further link a previously described sequence motif enriched in European recombination hotspots to the presence of a common PRDM9 zinc-finger array allele (RPT6a). Together, our results demonstrate functional differences between PRDM9 alleles which contribute to divergence in recombination landscapes in Atlantic salmon, paralleling patterns observed in mammals. The broad geographic distribution of Atlantic salmon, combined with extensive pedigree data generated through aquaculture, highlights its potential as a powerful model for studying PRDM9 function and evolution beyond mammals.
]]></description>
<dc:creator><![CDATA[ Gulbrandsen, O. S., Brekke, C., Baudement, M.-O., Nguyen, T. T., Kent, M. P., Barson, N. J., Lien, S. ]]></dc:creator>
<dc:date>2026-09-09</dc:date>
<dc:identifier>doi:10.64898/2026.09.03.749262</dc:identifier>
<dc:title><![CDATA[PRDM9 Alleles Guide Distinct Patterns of Recombination Localization in Atlantic Salmon]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.04.749300v1?rss=1">
<title>
<![CDATA[
Transcription-Coupled Chromatin Reinforcement Maintains the Mature Cardiomyocyte State 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.04.749300v1?rss=1
</link>
<description><![CDATA[
Chromatin homeostasis is fundamental to maintaining transcriptional programs that stabilize cell states while permitting plasticity for timely state transitions. However, mechanisms that actively sustain mature cell states after their establishment remain poorly defined despite being essential for lifelong maintenance of specialized cellular functions. Here we demonstrate that the transcription-coupled chromatin regulator RNF20 is crucial for maintaining chromatin accessibility at identity-associated promoters that support mature cardiomyocyte transcriptional programs in adult murine cardiomyocytes. Depletion of RNF20 progressively erodes the transcriptional, structural, and functional integrity of adult cardiomyocytes and activates AP-1-associated stress-responsive enhancer elements without cell-cycle re-entry. Spatial transcriptomics further revealed a subendocardial localization of this stress-responsive state. Together, these findings support a model in which transcription-coupled chromatin reinforcement continuously stabilizes the mature cardiomyocyte attractor state while constraining transitions toward pathological cell states.
]]></description>
<dc:creator><![CDATA[ Tang, H.-H., Tseng, H.-Y., Lin, C.-Y., Kao, C.-F. ]]></dc:creator>
<dc:date>2026-09-08</dc:date>
<dc:identifier>doi:10.64898/2026.09.04.749300</dc:identifier>
<dc:title><![CDATA[Transcription-Coupled Chromatin Reinforcement Maintains the Mature Cardiomyocyte State]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-08</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.04.749549v1?rss=1">
<title>
<![CDATA[
Genetic trans-effects link triglyceride-rich lipoproteins to blood pressure 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.04.749549v1?rss=1
</link>
<description><![CDATA[
Background: Genome-wide association studies (GWASs) have identified thousands of genomic regions in which common variants affect blood pressure, but have yielded limited mechanistic insight. This study used a novel method of genetic analysis based on identifying core genes on which the _trans_-effects of common variants coalesce to influence blood pressure. Methods: We undertook GWASs of mean arterial pressure (MAP) and body mass index (BMI) in 373,882 individuals aged less than 60 years in the Our Future Health study. We used summary statistics from GWASs of proteins on the SomaScan and Olink platforms to compute genome-wide aggregated trans-effects (GATE) scores for each protein, and tested for association of MAP with these scores. Results: The strongest GATE score association with MAP was for lipoprotein lipase (LpL, encoded by LPL_. Genetic up-regulation of circulating levels of LpL was associated with lower MAP but higher BMI. Associations of MAP and BMI with GATE scores for circulating levels of proteins encoded by three other genes involved in lipid handling -- CD300LG, ADIPOQ, TIMP4 -- were similar to those with LpL. GATE scores for all four of these proteins were inversely associated with measurements by NMR spectroscopy of plasma triglyceride in chylomicrons and extremely large VLDL particles. Conclusions: These results point to a key role in hypertension for proteins that regulate post-prandial clearance of triglyceride-rich lipoproteins, independently of adiposity. This is consistent with experimental studies showing that accumulation of lipids in endothelial cells impairs endothelial function.
]]></description>
<dc:creator><![CDATA[ Braichenko, S., Iakovliev, A., Dyer, J., Zhou, X., Spiliopoulou, A., Colhoun, H. M., McKeigue, P. ]]></dc:creator>
<dc:date>2026-09-08</dc:date>
<dc:identifier>doi:10.64898/2026.09.04.749549</dc:identifier>
<dc:title><![CDATA[Genetic trans-effects link triglyceride-rich lipoproteins to blood pressure]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-08</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.04.749340v1?rss=1">
<title>
<![CDATA[
Bundling Alleles Within Haplotype Blocks Improves QTL Detection Under Allelic Heterogeneity 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.04.749340v1?rss=1
</link>
<description><![CDATA[
Allelic heterogeneity is a term from genetics which means that alleles that differ in primary sequence can have a similar phenotypic outcome. In other words, they are functional equivalents, and they naturally appear through convergent evolution under selection. Current GWAS has trouble detecting these instances, as allelic heterogeneity leads to signal dilution in these analyses, often leading to a LOD score that stays below detection thresholds. In this paper, we show a method that can overcome this problem by bundling haplotypes into Artificial Combined Markers. The created marker matrix can then easily be used in existing GWAS software.
]]></description>
<dc:creator><![CDATA[ Oome, S., Ghanbari, M. ]]></dc:creator>
<dc:date>2026-09-08</dc:date>
<dc:identifier>doi:10.64898/2026.09.04.749340</dc:identifier>
<dc:title><![CDATA[Bundling Alleles Within Haplotype Blocks Improves QTL Detection Under Allelic Heterogeneity]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-08</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.03.749261v1?rss=1">
<title>
<![CDATA[
Synonymous HTT CAA/CCA-loss variants associated with early Huntington disease onset enhance toxicity beyond somatic instability 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.03.749261v1?rss=1
</link>
<description><![CDATA[
Huntington disease is a fatal neurodegenerative disorder caused by CAG repeat expansion encoding polyglutamine in the HTT gene. Recent studies have shown that loss of CAA/CCA interruptions within polyglutamine-coding CAG tracts and adjacent polyproline-coding region are linked to earlier disease onset. It has been hypothesized that somatic repeat instability, influenced by these interrupted CAG tracts, may mediate this effect. Here we demonstrate that HTT CAA/CCA-loss variant linked to early disease onset exacerbates mutant HTT toxicity in cellular models through mechanisms independent of somatic repeat instability. The CAA/CCA-loss variant exhibits significantly higher toxicity than canonical HTT sequences in both transient expression and stable cell line models. Notably, this enhanced toxicity persists in knockout cells of the mismatch repair gene MSH3 where somatic instability is blunted, with a consistent toxicity hierarchy (CAA/CCA-loss > CCA-loss > CAA-loss > canonical HTT) in both wildtype and MSH3 knockout cells. Furthermore, the CAA/CCA-loss variant generates elevated levels of repeat-associated non-AUG (RAN) translation products. In HEK293-based cellular models, these results suggest that the disease-accelerating effects of HTT CAA/CCA-loss variants involve intrinsic properties of the altered sequence context, highlighting the importance of understanding sequence-specific mechanisms in HD pathogenesis beyond polyglutamine length and somatic instability.
]]></description>
<dc:creator><![CDATA[ Sequiera, G. L., Gjervan, S. C., McCallum, R., Feng, J., Ozgoren, O. K., Bergh, S., Begin, J., Levesley, J., Findlay Black, H., Kay, C., Soomarooah, T., Arning, L., Rajan Babu, I. S., Basak, A. N., Klempir, J., Nguyen, H. P., Petersen, A., Hayden, M. R., Pouladi, M. A. ]]></dc:creator>
<dc:date>2026-09-08</dc:date>
<dc:identifier>doi:10.64898/2026.09.03.749261</dc:identifier>
<dc:title><![CDATA[Synonymous HTT CAA/CCA-loss variants associated with early Huntington disease onset enhance toxicity beyond somatic instability]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-08</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.07.749888v1?rss=1">
<title>
<![CDATA[
Cell Geometry and Junction Arrangement Define the Mechanical Robustness of Plant Tissues 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.07.749888v1?rss=1
</link>
<description><![CDATA[
Plant tissues are composed of immobile, pressurised cells that must maintain structural integrity under diverse environmental loads. Unlike animal tissues, which adapt through cellular rearrangement, plants must achieve mechanical robustness through the geometric configuration of their cellular networks. In this study, we establish a mechanistic link between cell geometry and mechanical resilience by integrating multilayer 3D mechanical simulations with cellular-resolution image analysis across a phylogenetically diverse panel of plant species, including Zea mays, Tradescantia zebrina, and Arabidopsis thaliana. We identify three-way junctions as fundamental mechanical elements that function as flexible hinges enabling mechanical strain accommodation in plant tissues. In contrast, four-way junctions are significantly stiffer and lack this strain-absorbing mechanism, providing a mechanical rationale for their biological avoidance. We also find that tissue material properties and strain response depend on edge lengths, cell layer, the degree of hexagonal shape, and turgor pressure response. These findings reveal the mechanism by which cell division patterns can actively tune tissue resilience to mechanical stress. This work provides new insights into the evolution of different cell shapes and offers clear principles for bio-inspired material science and tissue engineering.
]]></description>
<dc:creator><![CDATA[ Smithers, E. T., Ejaz, M., Lenz, M. O., Serra, L., Laruelle, E., Robinson, S. ]]></dc:creator>
<dc:date>2026-09-08</dc:date>
<dc:identifier>doi:10.64898/2026.09.07.749888</dc:identifier>
<dc:title><![CDATA[Cell Geometry and Junction Arrangement Define the Mechanical Robustness of Plant Tissues]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-08</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.04.749482v1?rss=1">
<title>
<![CDATA[
Polar auxin transport regulates initial auxin patterning and polar nuclear migration during lateral root initiation 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.04.749482v1?rss=1
</link>
<description><![CDATA[
In Arabidopsis thaliana, local auxin accumulation in xylem-pole pericycle (XPP) cells specifies lateral root founder cells, which establish de novo cell polarity manifested by polar nuclear migration and subsequent asymmetric division. Here, we developed a fast-maturing, XPP/early lateral root primordium (LRP)-specific R2D2 auxin reporter (fx-R2D2) to visualize auxin dynamics with high spatiotemporal resolution during LRP initiation. We demonstrate that auxin increases broadly on the convex side of XPP during root bending. Within this region, cells showing particularly strong auxin responses emerged, and subsequently underwent polar nuclear migration and asymmetric division, initiating an LRP. When two LRPs initiated in close proximity, auxin levels in one rapidly decreased after the cell division, followed by cessation of further division. These findings provide a clear picture of auxin dynamics during LRP initiation. Under uniform auxin treatment, de novo LRP formation events occur. Auxin treatment initially induced a uniform auxin response at a high level, followed by localized auxin depletion in regions where LRPs did not subsequently form, demonstrating that auxin depletion as well as accumulation shapes the auxin patterns during LRP initiation. Furthermore, we reveal that local PIN-mediated polar auxin transport regulates both de novo auxin patterning and polar nuclear migration during LRP initiation.
]]></description>
<dc:creator><![CDATA[ Kaneta, S., Kakimoto, T. ]]></dc:creator>
<dc:date>2026-09-08</dc:date>
<dc:identifier>doi:10.64898/2026.09.04.749482</dc:identifier>
<dc:title><![CDATA[Polar auxin transport regulates initial auxin patterning and polar nuclear migration during lateral root initiation]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-08</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.04.749384v1?rss=1">
<title>
<![CDATA[
A cross-kingdom interactome predicted by AlphaFold3 reveals a DNF2-centered interface required for symbiotic accommodation 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.04.749384v1?rss=1
</link>
<description><![CDATA[
Legumes convert atmospheric nitrogen into ammonium through symbiotic bacteria housed in root nodules, yet the molecular interactions between rhizobial and host proteins inside nodules remain poorly understood. Here we employed AlphaFold3 to construct a cross-kingdom interactome between Medicago truncatula and its symbiont Sinorhizobium meliloti. Screening more than 217,000 protein pairs yielded 7,137 putative interactions, providing a valuable resource for the broader symbiosis community. Within this network, we focused on DEFECTIVE IN NITROGEN FIXATION 2 (DNF2), a host protein required for rhizobial persistence within nodules. We showed that DNF2 localizes to the peribacteroid space and associates with previously uncharacterized secreted rhizobial proteins (SRPs), suggesting it may function as a hub for host-symbiont communication. Notably, knockout of two DNF2-interacting proteins, SRP86 and SRP485, results in white, nitrogen-fixation-deficient nodules with abnormal symbiosomes and elevated expression of senescence-associated genes, closely phenocopying the dnf2 loss-of-function mutant. Together, our findings define a DNF2-SRP molecular framework underlying symbiotic accommodation, and illustrate the potential of AI-guided interactome mapping to uncover molecular mechanisms of plant-microbe interactions with relevance to sustainable agriculture.
]]></description>
<dc:creator><![CDATA[ Gao, J.-P., Zhao, F., Zhang, G., Chen, Q., Wu, S., Huang, J., Liu, C., Wang, G., Yu, P., Eves-van den Akker, S., Tian, C.-F., Ott, T., Murray, J., Oldroyd, G., Liang, P., Xia, C. ]]></dc:creator>
<dc:date>2026-09-08</dc:date>
<dc:identifier>doi:10.64898/2026.09.04.749384</dc:identifier>
<dc:title><![CDATA[A cross-kingdom interactome predicted by AlphaFold3 reveals a DNF2-centered interface required for symbiotic accommodation]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-08</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.04.749431v1?rss=1">
<title>
<![CDATA[
Base editing of EIF4E creates novel resistance alleles against bymoviruses in winter barley 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.04.749431v1?rss=1
</link>
<description><![CDATA[
The barley yellow mosaic virus disease is one of the most important threats of barley production in Europe and Asia. Transmitted by the soil-borne plasmodiophorid Polymyxa graminis, there are no direct control options against the causal bymoviruses Barley Yellow Mosaic Virus (BaYMV) and Barley Mild Mosaic Virus (BaMMV). Resistance breeding is thus the only viable approach and has been very successful in the past, with the resistance-conferring alleles rym4 and rym5 of the EUKARYOTIC TRANSLATION INITIATION FACTOR 4E being used extensively in European winter barley breeding. However, virus strains have meanwhile overcome this resistance. Therefore, there is an urgent need for new sources of resistance. Genome editing with Cas endonucleases is a timely and promising approach in this respect. However, the small insertions and deletions that frequently arise during site-directed mutagenesis usually lead to the knockout of the target genes. In the case of EIF4E, loss-of-function is accompanied by significant yield reduction. Consequently, more precisely edited alleles with retained function are necessary for crop improvement. The present study represents the first application of base editing in barley plants, using the EIF4E gene as an example. Base exchanges were made at two positions in this gene using an nCas9-cytidine deaminase fusion, resulting in a total of 10 novel EIF4E alleles in addition to the introduction of a single nucleotide polymorphism that is part of rym4. Two of these newly generated alleles led to resistance upon BaMMV inoculation without adverse effects on yield, proving this approach promising to generate new material for resistance breeding.
]]></description>
<dc:creator><![CDATA[ Hoffie, R. E., Habekuss, A., Perovic, D., Hoffie, I., Ordon, F., Kumlehn, J. ]]></dc:creator>
<dc:date>2026-09-08</dc:date>
<dc:identifier>doi:10.64898/2026.09.04.749431</dc:identifier>
<dc:title><![CDATA[Base editing of EIF4E creates novel resistance alleles against bymoviruses in winter barley]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-08</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.02.748655v1?rss=1">
<title>
<![CDATA[
ACHT2 deactivates carbon assimilation during light-dark transition 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.02.748655v1?rss=1
</link>
<description><![CDATA[
In chloroplasts, photosynthetic efficiency relies on a delicate balance between reductive and oxidative thiol-based signaling networks. Members of the high-midpoint-potential atypical thioredoxins (Trxs) were shown to oxidize photosynthetic enzymes by channeling reducing equivalents to H2O2 through 2-Cys-Prx activity. However, it remains unclear which atypical-Trx isoforms regulate Calvin-Benson cycle (CBC) inactivation, and whether they possess distinct functional specificities or operate redundantly in vivo. To resolve this, electron transport and carbon assimilation were continuously monitored during physiological dynamic light transitions in CRISPR-generated single, double and triple atypical Trx mutants. Notably, ACHT2 was identified as a primary determinant of CBC inactivation during dark-to-light transitions, as evidenced by the alleviation of redox-mediated bottlenecks in electron flow downstream of Fd and a lower CBC inactivation state in acht2 plants, resembling the phenotype observed in plants lacking 2-Cys Prxs A and B (2cpab). In contrast, plants mutated in ACHT1, ACHT4, or TrxL2 displayed CBC inactivation kinetics comparable to those of the wild type. Furthermore, mutation of ACHT2 did not compromise plant fitness. In contrast, growth retardation was observed in the acht1/acht4 double mutant, suggesting that the severe phenotype of 2cpab does not arise from impaired CBC inactivation, but rather from disruption of oxidative regulation of other metabolic pathways mediated by distinct atypical Trxs. Collectively, these findings reveal a high degree of regulatory specificity within the chloroplast oxidative network and provide a foundation for a deeper understanding of how activation-inactivation cycles contribute to plant adaptation to dynamic light environments.
]]></description>
<dc:creator><![CDATA[ Steinberg, M., Hipsch, M., Keisar, M., Lampl, N., Rosenwasser, S. ]]></dc:creator>
<dc:date>2026-09-07</dc:date>
<dc:identifier>doi:10.64898/2026.09.02.748655</dc:identifier>
<dc:title><![CDATA[ACHT2 deactivates carbon assimilation during light-dark transition]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.03.749275v1?rss=1">
<title>
<![CDATA[
Dynamic Filament Assembly Regulates the Prolyl Aminopeptidase Activity of Plant Immune Protein DM3 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.03.749275v1?rss=1
</link>
<description><![CDATA[
The alpha/beta hydrolase DANGEROUS MIX 3 (DM3), a proline aminopeptidase in Arabidopsis thaliana, contributes to stress resilience through both metabolic regulation and immune signaling. Its functions are partitioned within its oligomeric structure as a trimer-of-dimers, in which the immune regulatory switch resides at the dimer interface. While the enzymatic activity of DM3 is not necessary for immune response, its activity to free prolines is critical to promote tolerance to salt and drought stress. However, how this activity is regulated has remained unclear. Here, we show that DM3 undergoes dynamic and reversible assembly into higher-order filaments in a salt-sensitive manner. The cryo-electron microscopy (EM) structure of filamentous DM3 reveals that the three-stranded helical filament arises from rearrangements of a planar hexamer into a tilted hexameric configuration. Notably, within these filaments, one of the catalytic residues is flipped out to disrupt the catalytic geometry, rendering the enzyme inactive. These findings establish filament assembly as a mechanism to sequester DM3 in an inactive state and suggest that the transition between distinct oligomeric states enables DM3 to coordinate its roles in biotic and abiotic stress responses.
]]></description>
<dc:creator><![CDATA[ Kim, N., Wan, W.-L., Tan, Y. Y., Jang, I.-C., Chae, E., Song, J.-J. ]]></dc:creator>
<dc:date>2026-09-07</dc:date>
<dc:identifier>doi:10.64898/2026.09.03.749275</dc:identifier>
<dc:title><![CDATA[Dynamic Filament Assembly Regulates the Prolyl Aminopeptidase Activity of Plant Immune Protein DM3]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.03.749138v1?rss=1">
<title>
<![CDATA[
The PP2A phosphatase associates with the Arabidopsis TRAPPII tethering complex and dephosphorylates a TRAPPII-derived phosphopeptide in vitro 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.03.749138v1?rss=1
</link>
<description><![CDATA[
The transport protein particle II (TRAPPII) complex is a conserved regulator of post-Golgi membrane trafficking. In Arabidopsis, phosphorylation of the TRAPPII-specific subunit TRS120 by SHAGGY-like kinases modulates adaptive growth responses, but the phosphatases that reverse this phosphorylation remain unknown. Here, proteomic analyses identified subunits of Protein Phosphatase 2A (PP2A) in the TRAPPII interactome. PP2A subunits physically associated with TRAPPII, and double-mutant analyses revealed genetic interactions between PP2A and TRAPPII. Loss of TRAPPII function reduced the relative membrane association of PP2A scaffolding subunits. We established an in vitro assay for Arabidopsis PP2A holoenzyme activity using complexes transiently co-expressed and affinity-purified from Nicotiana benthamiana. Structural modelling and interface analysis predicted binding of a phosphorylated peptide encompassing a TRS120 phosphosite cluster at the PP2A catalytic interface, while biochemical assays showed that a PP2A holoenzyme containing the B2 regulatory subunit dephosphorylated this peptide. Together, these findings identify a B2-containing PP2A holoenzyme as a candidate phosphatase for TRS120 and support a model in which antagonistic SHAGGY-like kinase and PP2A activities couple signalling to membrane trafficking during plant development and environmental adaptation.
]]></description>
<dc:creator><![CDATA[ Strohmayr, A., Steiner, A., Wiese, C., Abele, M., Facher, E., Belcram, K., Altmann, M., Falter-Braun, P., Ludwig, C., Pastuglia, M., Bouchez, D., Assaad, F. F. ]]></dc:creator>
<dc:date>2026-09-07</dc:date>
<dc:identifier>doi:10.64898/2026.09.03.749138</dc:identifier>
<dc:title><![CDATA[The PP2A phosphatase associates with the Arabidopsis TRAPPII tethering complex and dephosphorylates a TRAPPII-derived phosphopeptide in vitro]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.04.749355v1?rss=1">
<title>
<![CDATA[
BOTANIC-1: a series of long-context plant genomic foundation models in the agentic era 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.04.749355v1?rss=1
</link>
<description><![CDATA[
The development of climate-resilient crops would be greatly accelerated by models able to reason directly over plant genomic sequences and to pinpoint trait-associated regions or loci. Anticipating the impact of DNA base changes (variants) remains challenging, and understanding regulatory mechanisms is still an active area of research. Through self-supervised training on unannotated genomic data, genomic language models (gLMs) can learn DNA syntax and grammar that go beyond current annotations, thus complementing standard bioinformatics analyses that rely on rules established by decades of genomics research. Here we present our agent-powered Model Factory and its first outputs: the Botanic1 family of gLMs designed for plant research, which operates reliably on sequences from hundreds of base pairs up to 128 kbp. These models outperform all generalist and plant-specific gLMs (as well as specialised baselines) on one of the largest sets of plant genomics evaluation tasks reported to date, at a much smaller budget than concurrent models. Mechanistic interpretability analysis identifies features associated with biologically meaningful sequence properties including coding region boundaries and splice site motifs, demonstrating that these models are a source of biological insight beyond their benchmark performance. Finally, because a gLM only becomes practically useful when embedded in a broader workflow, we integrate Botanic1 as a specialised genomic layer callable by a generalist large language model (LLM) agent, illustrating how such hybrid systems could accelerate plant biology research. To support the plant genomics research community, we release the four Botanic1 models, their pre-training corpus and the trained sparse autoencoder for research use at https://huggingface.co/spaces/living-models/botanic1-report.
]]></description>
<dc:creator><![CDATA[ Barozet, A., Cabeli, V., Ogier du Terrail, J., Rukhovich, A., Janssoone, T., Klajer, G., Sheikhitarghi, Z., Andrews, G., Veran, C., Strouk, L. ]]></dc:creator>
<dc:date>2026-09-07</dc:date>
<dc:identifier>doi:10.64898/2026.09.04.749355</dc:identifier>
<dc:title><![CDATA[BOTANIC-1: a series of long-context plant genomic foundation models in the agentic era]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.03.745400v1?rss=1">
<title>
<![CDATA[
Continuous monitoring of deficit irrigation in avocado across two contrasting rainfall years using sensor networks, telemetry, and machine learning 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.03.745400v1?rss=1
</link>
<description><![CDATA[
Water scarcity and increasingly irregular rainfall threaten avocado production in Mediterranean regions, yet the long term physiological responses of mature trees to sustained deficit irrigation remain poorly understood. We conducted a two-year field study integrating continuous monitoring of the soil plant atmosphere continuum, drone-based multispectral imaging, canopy structural analysis, and fruit phenotyping in a mature avocado orchard subjected to three irrigation regimes. The two study years differed markedly in rainfall, providing a unique opportunity to evaluate how environmental conditions modulate tree responses to water limitation. Trees under severe deficit irrigation showed depletion of water in deeper soil layers and a flattened physiological profile, with near-zero diel variation in leaf thickness and trunk water potential, indicating minimal transpiration and decoupling of tree water status from environmental demand. Drone telemetry via NDVI detected stress during fruit growth and maturation, but not during flowering or the new summer leaf flush, revealing greater drought sensitivity at later maturation stages. Although canopy area did not differ among irrigation treatments, canopy surface roughness increased significantly under deficit irrigation, thereby identifying a novel structural indicator of drought stress. Despite large physiological differences among treatments, fruit number remained stable, while fruit weight decreased significantly under severe deficit irrigation, particularly in the wetter year, suggesting that annual rainfall modulates the trade-off between fruit retention and fruit growth. This study provides the first continuous, multi-scale characterization of avocado performance under sustained deficit irrigation in Mediterranean conditions. By integrating plant-based sensors, remote sensing, and artificial intelligence, we reveal previously undescribed stress dynamics and identify new indicators for precision irrigation management in fruit crops.
]]></description>
<dc:creator><![CDATA[ Ferez-Gomez, A., Soler-Escamez, L., Ferrer-Blanco, C., Perez-Aguilar, A., Hormaza, J. I., Diaz-Zayas, A., Losada, J. M. ]]></dc:creator>
<dc:date>2026-09-07</dc:date>
<dc:identifier>doi:10.64898/2026.09.03.745400</dc:identifier>
<dc:title><![CDATA[Continuous monitoring of deficit irrigation in avocado across two contrasting rainfall years using sensor networks, telemetry, and machine learning]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.03.749126v1?rss=1">
<title>
<![CDATA[
Endogenous and environmentally modulated leaf shape plasticity in Boquila trifoliolata: how good is the evidence for mimicry? 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.03.749126v1?rss=1
</link>
<description><![CDATA[
Reports that the South American climbing vine Boquila trifoliolata modifies its leaf shape to mimic leaves of its host plant have raised considerable attention. Boquila leaf development was proposed to reflect visual inputs perceived in an unknown manner. However, the very existence of Boquila leaf shape mimicry remains inconclusive, since the reported observations are open to alternative explanations. We performed an initial quantitative characterization of leaf shape variability in glasshouse-cultured clonal Boquila plants grown without close host contact, and attempted to reproduce the leaf shape mimicry phenomenon under controlled culture conditions using live olive (Olea europaea) plants, artificial (decoy) olive or artificial ivy plants as supports. While we found leaves of variable shape (including those resembling ivy leaves) both in plants grown without host contact and in those climbing on live or decoy hosts, we did not observe any link between leaf shape and host presence or character. Instead, the leaf shape appears to be affected by environmental conditions including the season. Although our study was limited to a single Boquila genotype and an ecologically unrealistic host selection, our observations suggest that the alleged mimicry might originate from unintentional misinterpretation of intrinsic discontinuous leaf shape plasticity in field observations.
]]></description>
<dc:creator><![CDATA[ Cvrckova, F., Sonka, J., Bezvoda, R., Krtkova, J., Konradova, H., Zarsky, V. ]]></dc:creator>
<dc:date>2026-09-07</dc:date>
<dc:identifier>doi:10.64898/2026.09.03.749126</dc:identifier>
<dc:title><![CDATA[Endogenous and environmentally modulated leaf shape plasticity in Boquila trifoliolata: how good is the evidence for mimicry?]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.03.749191v1?rss=1">
<title>
<![CDATA[
Provitamin A maize inbred lines exhibit resistance to multiple foliar diseases under laboratory and field conditions 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.03.749191v1?rss=1
</link>
<description><![CDATA[
Maize (Zea mays) is a staple food for millions in sub-Saharan Africa (SSA), contributing to both caloric intake and essential micronutrients. Recent breeding efforts have focused on enhancing its nutritional value by increasing provitamin A (PVA) carotenoid content to address vitamin A deficiency (VAD), a common problem among children under 5 years, pregnant and lactating mothers across SSA. However, high rainfall, and both warm and humid conditions in various SSA regions result in devastating foliar diseases such as maize streak virus (MSV), northern corn leaf blight (NCLB), southern corn leaf blight (SCLB), southern corn rust, grey leaf spot (GLS), and Curvularia leaf spot (CLS). Breeding for resistance can aid in mitigating yield losses caused by those diseases. Rapid, efficient screening methods can allow for examining large germplasm collections. The current study evaluated 21 maize inbred lines with contrasting PVA content, along with two commercial inbred controls, for resistance to Exserohilum turcicum, Bipolaris maydis, and Curvularia lunata, causal agents of NCLB, SCLB, and CLS, respectively, using a detached leaf assay (DLA) and under natural field infestation. Significant variation was detected among the inbreds, seven were classified as resistant to certain diseases, ten as moderately resistant, and six as susceptible to all foliar diseases. Overall, high PVA inbred lines had less susceptibility to NCLB, SCLB, and CLS. The results suggest that PVA-enriched maize inbred lines possess improved resistance to multiple foliar diseases. The field assessments of disease severity validated the effectiveness of the DLA in distinguishing resistant from susceptible inbred lines, and resistance to other diseases in field conditions was detected in parallel. The results indicate that high PVA maize has the potential to simultaneously address VAD, mycotoxin contamination in SSA with improved resistance to multiple foliar diseases.
]]></description>
<dc:creator><![CDATA[ Mboup, M., Aduramigba-Modupe, A. O., Olasanmi, B., Mengesha, W., Meseka, S., Dieng, I., Menkir, A., Ortega-Beltran, A. ]]></dc:creator>
<dc:date>2026-09-07</dc:date>
<dc:identifier>doi:10.64898/2026.09.03.749191</dc:identifier>
<dc:title><![CDATA[Provitamin A maize inbred lines exhibit resistance to multiple foliar diseases under laboratory and field conditions]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.03.749270v1?rss=1">
<title>
<![CDATA[
Duckweeds as Multiplexable Plant Models for Exploring Abiotic Stress Responses 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.03.749270v1?rss=1
</link>
<description><![CDATA[
In nature, plants experience complex combinations of environmental stresses. Prior studies using Arabidopsis thaliana show that transcriptional responses to combinatorial stress are unique and cannot be predicted from responses to individual treatments, making it imperative to study combinatorial stress in the monocotyledonous cereals that comprise the majority of our food supply. However, crop species are not easily amenable for such studies because of their large size, long generation time, and organismal complexity. In contrast, the monocotyledonous aquatic duckweeds are small, grow rapidly, and show reduced organismal and genomic complexity. Here, we explore the physiological responses to combinatorial stress in three duckweed species, S. polyrhiza, L. minor, and W. australiana and examine their potential to serve as multiplexable models. Focusing on S. polyrhiza, the most complex and best annotated species, we investigated transcriptional response to individual and combinatorial stress treatments. While most individual treatments elicit few transcriptional changes, combinatorial stress elicited a non-additive transcriptional response unique to each combination. Exploring the duckweed regulatory landscape, we found that regulatory regions near genes that were differentially expressed in combinatorial stress in S. polyrhiza resemble environmentally responsive regulatory elements found in terrestrial plants. Examined duckweed species show numbers and genomic distributions of regulatory elements similar to those of A. thaliana and maize, with subtle effects of genome size but none of organismal complexity. Taken together, our results establish that duckweeds respond to combinatorial stress in a manner similar to terrestrial plants and can therefore serve as high-throughput, multiplexable models for studying its molecular underpinnings.
]]></description>
<dc:creator><![CDATA[ Ramirez-Corona, B., Cadena, S., Bubb, K. L., Queitsch, C., Cuperus, J. ]]></dc:creator>
<dc:date>2026-09-07</dc:date>
<dc:identifier>doi:10.64898/2026.09.03.749270</dc:identifier>
<dc:title><![CDATA[Duckweeds as Multiplexable Plant Models for Exploring Abiotic Stress Responses]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.04.749343v1?rss=1">
<title>
<![CDATA[
Genetic dissection of a Solanum elaeagnifolium tertiary genepool introgression associated with 4-O-caffeoylquinic acid accumulation in eggplant 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.04.749343v1?rss=1
</link>
<description><![CDATA[
Caffeoylquinic acids (CQAs) are the major phenolic compounds in eggplant (Solanum melongena) fruit, with 5-O-caffeoylquinic acid (5-CQA; chlorogenic acid) as the predominant isomer, while crop wild relatives may offer novel variation for diversifying these profiles. Previous work detected a distinct phenolic acid profile in S. elaeagnifolium, a tertiary genepool wild relative of eggplant, and in advanced backcross materials carrying introgressions from this species. This profile was characterized by a secondary chromatographic peak eluting after 5-CQA, but the identity of this compound and the associated chromosome 1 region remained unresolved. Here, we combined HPLC-MS-based metabolite identification, fine mapping, and comparative microsynteny analysis to characterize this phenotype. The secondary peak was identified as 4-O-caffeoylquinic acid (4-CQA). Fine mapping across three consecutive selfing generations, involving 612 screened individuals and 21 informative recombinants, reduced the associated interval from 2.753 Mb to 0.211 Mb, delimiting a region containing 30 annotated genes. The 4-CQA peak was detected in both homozygous and heterozygous introgression-derived materials, consistent with dominant control of the trait. Structural comparison of the fine-mapped interval revealed broad conservation between S. melongena and S. elaeagnifolium, but also identified a localized structurally divergent block potentially underlying the secondary 4-CQA peak. Within this block, the S. elaeagnifolium interval harbors acetylajmalan esterase-like/GDSL-type genes and a transcript-supported putative novel donor-specific gene. Overall, this study highlights S. elaeagnifolium introgressions as a promising source of phenolic diversification and providing markers to facilitate the development of eggplant lines with a more diverse CQA profile and potentially enhanced functional quality.
]]></description>
<dc:creator><![CDATA[ Villanueva, G., Rosa-Martinez, E., Moreno, D. A., Gramazio, P., Baraja-Fonseca, V., Vilanova, S., Prohens, J., Plazas, M. ]]></dc:creator>
<dc:date>2026-09-07</dc:date>
<dc:identifier>doi:10.64898/2026.09.04.749343</dc:identifier>
<dc:title><![CDATA[Genetic dissection of a Solanum elaeagnifolium tertiary genepool introgression associated with 4-O-caffeoylquinic acid accumulation in eggplant]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.03.748596v1?rss=1">
<title>
<![CDATA[
Sexual dimorphism of autism-like phenotypes in microglial eIF4E overexpression mice 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.03.748596v1?rss=1
</link>
<description><![CDATA[
Background: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by deficits in social communication and interaction, and restricted interests or repetitive behaviors. ASD is approximately four times more prevalent in males than in females. In this study, we investigated whether sex hormones or sex chromosomes underlie the male bias in ASD susceptibility. Methods: We used the MG4E mouse model, in which microglial eIF4E overexpression produces robust male-biased ASD-like phenotypes. To distinguish the contributions of sex hormones and sex chromosomes, MG4E mice were crossed with four-core-genotype (FCG) mice carrying Sry gene manipulations, generating eight genotypes of experimental mice. Social interaction and repetitive behaviors were assessed using standard behavioral assays. Dendritic spine density was quantified in Thy1-GFP mice. Expression of estrogen receptors (ERs) and androgen receptor (AR) was examined in microglia isolated from control and MG4E mice. Results: Sex hormones, rather than non-Sry genes on sex chromosomes, are responsible for the male-biased deficits in social interaction and the increase in dendritic spine density. At postnatal day 14, ERs were undetectable in microglia, whereas ER expression was readily detected in neurons. Conclusions: These findings demonstrate that sex hormones are a major determinant of the increased susceptibility of males to ASD-like phenotypes in MG4E mice. The absence of ER expression in microglia suggests that sex hormones may act indirectly through hormone-responsive neurons to regulate microglia-neuron interactions during neurodevelopment.
]]></description>
<dc:creator><![CDATA[ Niu, C., An, J. J., Masterson, H. V., Xu, B. ]]></dc:creator>
<dc:date>2026-09-07</dc:date>
<dc:identifier>doi:10.64898/2026.09.03.748596</dc:identifier>
<dc:title><![CDATA[Sexual dimorphism of autism-like phenotypes in microglial eIF4E overexpression mice]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.01.748516v1?rss=1">
<title>
<![CDATA[
Phantom genetic nurture: assortative mating accounts for most of the apparent association between parental genotypes and childhood cognitive performance 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.01.748516v1?rss=1
</link>
<description><![CDATA[
Parental genotypes may influence offspring outcomes through the environments parents provide, a process known as genetic nurture, but estimating such effects from polygenic scores is complicated jointly by measurement error, unobserved genetic variation, and assortative mating. Here, we introduce RAVEL, a structural equation modeling framework that uses two independently constructed polygenic scores for the same trait to estimate latent genetic liability associations in parent-offspring trios and to distinguish direct and non-transmitted genetic associations. Through analytic derivations and simulations, we show that naive trio regressions can produce spurious non-zero parental coefficients, attenuate genuine genetic nurture effects, and obscure asymmetric parental effects, whereas RAVEL recovers unbiased estimates of the underlying coefficients when the assortative mating history and the extent of unobserved genetic variation are correctly specified. Applying RAVEL to national test scores in the Norwegian Mother, Father and Child Cohort Study using polygenic scores for educational attainment, we find that parental genetic liabilities explain less than 0.5% as much variance in childhood cognitive performance as the child's own genetic liability (substantially lower than the 10% observed with naive trio regressions) once assortative mating is modeled, with only a small paternal association significantly surviving the correction. In contrast, we find a maternal-specific non-transmitted association with offspring premature birth. RAVEL provides a general framework for interpreting trio polygenic score analyses of direct and non-transmitted genetic effects, clarifying the contribution of parental genetic liabilities to offspring traits.
]]></description>
<dc:creator><![CDATA[ Malawsky, D. S., Hegemann, L., Wootton, O., Havdahl, A. K., Sunde, H. F., Martin, H. C. ]]></dc:creator>
<dc:date>2026-09-06</dc:date>
<dc:identifier>doi:10.64898/2026.09.01.748516</dc:identifier>
<dc:title><![CDATA[Phantom genetic nurture: assortative mating accounts for most of the apparent association between parental genotypes and childhood cognitive performance]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-06</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.03.749093v1?rss=1">
<title>
<![CDATA[
Spatiotemporal pectin remodelling, glycoproteins, and LEA proteins maintain cell wall integrity during desiccation and rehydration in Ramonda serbica 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.03.749093v1?rss=1
</link>
<description><![CDATA[
Vegetative desiccation tolerance requires specialised cell wall (CW) adaptations to withstand severe mechanical stress during dehydration and rehydration. While intracellular protective strategies in resurrection plants, including Ramonda serbica, are well documented, the CW response remains poorly understood. Here, we integrated immunocytochemical profiling, FTIR spectroscopy, quantification of CW-bound phenolics, transcriptomics, and ionically bound CW proteomics across hydrated (HL), desiccated (DL), and rehydrated states (R1-1h, R2-24h, R3-48h). Reversible CW folding was facilitated by condensed arabinogalactan-proteins (AGPs) and extensins, alongside a site-specific balance between pectin methylesterification and demethylesterification. Structural compaction was further reinforced by the accumulation of CW-bound hydroxycinnamates, which persisted through R1 phase. Moreover, basic 7S globulin, miraculin, -galactosidase, and two LEA4 protein family members were strongly accumulated during DL and R1, providing the first evidence of ionically CW-bound LEA proteins. Initial rewatering (R1) triggered a rapid transcriptomic reactivation of pectin-degrading/modifying enzymes, carbohydrate-active enzymes, and subtilases, accompanied by unesterified pectin enrichment. By 24-48 h (R2-R3), CW-bound hydroxycinnamic acids declined, and CW architecture, gene expression, and proteome profiles returned to baseline levels. Overall, our findings reveal a coordinated spatiotemporal apoplastic network - driven by glycoproteins, pectin modulation, CW-bound hydroxycinnamates, and LEA4 proteins - essential for rapid desiccation recovery.
]]></description>
<dc:creator><![CDATA[ Pantelic, A., Ilina, T., Milic, D., Kutyrieva-Nowak, N., Lekic, S., Popovic, L., Balliau, T., Vujisic, L., Leszczuk, A., Blein-Nicolas, M., Vidovic, M. ]]></dc:creator>
<dc:date>2026-09-06</dc:date>
<dc:identifier>doi:10.64898/2026.09.03.749093</dc:identifier>
<dc:title><![CDATA[Spatiotemporal pectin remodelling, glycoproteins, and LEA proteins maintain cell wall integrity during desiccation and rehydration in Ramonda serbica]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-06</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.01.748656v1?rss=1">
<title>
<![CDATA[
Conditions and properties of non-Mendelian transmission of recombinants in female meiosis 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.01.748656v1?rss=1
</link>
<description><![CDATA[
In female meiosis, each of the four chromatids in a tetrad has a 25% chance to be selected for transmission through the pronucleus, realizing Mendel's second law. Here, we characterize a cheating but unselfish behaviour that has documented cases across diverse animal taxa including humans and flies, whereby chromatids with crossovers (COs) have a transmission advantage, resulting in increased production of recombinant offspring. Taking advantage of Drosophila ovarian physiology, we show that this form of meiotic cheating which we call recombinant drive occurs on the autosomes when females are under nutrient stress, potentially as a mechanism for recombination plasticity, while curiously, the effect is suppressed on the X by the distributive system. We explored recombinant drive using simulations and identified unique quantitative signatures that are at odds with several intrinsic properties of linkage. One violation is the production of more offspring with recombinant versus parental allele combinations, which we empirically demonstrated to be possible. Further, we show that recombinant drive can appear to modify CO patterning effectively acting as assurance and interference mechanisms, even when it has no influence on and acts downstream of CO spacing. We discuss the potential benefits and consequences of having a conserved method that can rapidly increase recombination in response to stress, and speculate on a mechanism for the preferential transmission of COs at meiosis II. Overall, our study revealed distinct properties and behaviours of a poorly understood, but potentially widespread, conserved phenomenon and offers avenues for broad detection and mechanistic dissection.
]]></description>
<dc:creator><![CDATA[ Chauhan, A., Yeung, N., Kim, H., Wei, K. ]]></dc:creator>
<dc:date>2026-09-05</dc:date>
<dc:identifier>doi:10.64898/2026.09.01.748656</dc:identifier>
<dc:title><![CDATA[Conditions and properties of non-Mendelian transmission of recombinants in female meiosis]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-05</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.01.748529v1?rss=1">
<title>
<![CDATA[
A large-effect locus on chromosome 4 underlies circadian feeding rhythmicity in pigs 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.01.748529v1?rss=1
</link>
<description><![CDATA[
Circadian feeding rhythmicity reflects the distribution of feed intake across the daily 24-hour cycle. Regular feeding-fasting cycles play an important role in regulating metabolism and maintaining health, but endogenous and environmental factors can disrupt the normal circadian pattern of feed intake. Here, we quantified hourly feed intake in 3,470 Swiss Landrace and 15,181 Swiss Large White pigs using 40.5 million records from automated feeding systems. We used the proportion of days exhibiting a significant feeding rhythm after wavelet analysis to investigate variation in circadian feeding organization. Circadian feeding rhythmicity was influenced by sex and age, with higher rhythmicity observed in females and older animals. Variance components analysis revealed a strong additive genetic contribution and a high heritability (0.53-0.57). Pigs with higher circadian feeding rhythmicity had reduced nocturnal intake, improved feed conversion ratio, and lower day-to-day variability in feed intake, suggesting improved feed efficiency and resilience. Genome-wide association testing of 15.7 and 23.1 million imputed sequence variants identified a QTL on chromosome 4 explaining 5.3% and 2.9% of the phenotypic variance of circadian feeding rhythmicity in Swiss Landrace and Swiss Large White pigs, respectively. The QTL overlaps OPRK1 and NPBWR1, two genes implicated in the regulation of feeding behavior, reward and energy homeostasis. Collectively, our findings establish circadian feeding behavior as a heritable trait in pigs and provide a basis to further investigate the genetic regulation of feeding rhythms in mammals and explore its use in animal breeding programs to improve feed efficiency and resilience.
]]></description>
<dc:creator><![CDATA[ Gorssen, W., Kadri, N., Mapel, X. M., Leonard, A. S., He, Q., Winters, C., Khayatzadeh, N., Kasper, C., Pausch, H. ]]></dc:creator>
<dc:date>2026-09-04</dc:date>
<dc:identifier>doi:10.64898/2026.09.01.748529</dc:identifier>
<dc:title><![CDATA[A large-effect locus on chromosome 4 underlies circadian feeding rhythmicity in pigs]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-04</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.02.748779v1?rss=1">
<title>
<![CDATA[
Wolf microevolution in the melting pot: range expansion, population sympatry, dynamic mosaic admixture zone and asymmetric gene flow 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.02.748779v1?rss=1
</link>
<description><![CDATA[
Here we describe substantial range shifts of historically differentiated wolf populations and formation of novel sympatric zones during the recent decade in Central Europe. This region provides a natural laboratory for testing alternative scenarios of population interactions from continued isolation or restricted gene flow to progressive population fusion, while prompting a reassessment of their geographic ranges. Based on sampling across the Czech Republic and Slovakia obtained from large-scale monitoring programmes over five wolf years (2020/21_2024/25), complemented by comparative material from neighbouring regions, we analysed mitochondrial haplotypes, autosomal microsatellite genotypes and sex-linked loci. The Central European population with Baltic ancestry predominated across large parts of Central Europe including the Bohemian Massif with enclaves in the Western Carpathians. The Carpathian population was predominant in Slovakia, with a smaller satellite occurrence in the northern part of the Bohemian Massif. Alpine population was centred in the Alps but extended into southern parts of Bohemian Massif and Central German Uplands. Following the sporadic occurrence of admixed individuals, broad mosaic and dynamic sympatric zones have formed in the Czech Republic and Slovakia in the last decade. These scenarios could be facilitated by the presence of intermediate habitats and isolation of the Bohemian Massif structural basin, framed by a massive ring fault system. Recent-immigration estimates are asymmetric, with the largest mean contributions from the Alpine to the Central European population and from the Central European to the Carpathian population, with the second case potentially linked to source-sink dynamics driven by the hunting pressure within the Carpathian population (whereas the others are protected year-round). Whether increasing admixture will enhance viability of populations (that currently have small effective sizes) through genetic rescue or carry risks of outbreeding depression remains uncertain, highlighting the need for continued transboundary monitoring within conservation biology framework.
]]></description>
<dc:creator><![CDATA[ Srutova, J., Tkacova, N., Cetkovska, E., Eliasova, K., Veselovska, L., Ungrova, L., Montoya, K., Skrobanek, M., Mateju, P., Dula, M., Vorel, A., Mokry, J., Mikslova, K., Collet, S., Nowak, C., Rolle, F., Marucco, F., Szewczyk, M., Myslajek, R., Nowak, S., Findo, S., Antal, V., Kutal, M., Jelinkova, J., Bolfikova, B. C., Hulva, P. ]]></dc:creator>
<dc:date>2026-09-04</dc:date>
<dc:identifier>doi:10.64898/2026.09.02.748779</dc:identifier>
<dc:title><![CDATA[Wolf microevolution in the melting pot: range expansion, population sympatry, dynamic mosaic admixture zone and asymmetric gene flow]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-04</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.02.748885v1?rss=1">
<title>
<![CDATA[
Evidence for a regulatory role of the evolutionarily conserved sequence complementarity between tRNAs 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.02.748885v1?rss=1
</link>
<description><![CDATA[
The tRNAs are non-coding RNAs (ncRNAs) known for their classical role in decoding mRNAs. Analysis of tRNA sequences from Escherichia coli revealed pairwise similarities for different combinations of tRNAs, as well as complementarities between some tRNA pairs. To explore the physiological significance of the complementarities between the tRNAs, we investigated the pair of tRNAs encoded by lysT (encoding an abundant tRNA, tRNALysT), and argU (encoding a rare tRNA, tRNAArgU). We show that tRNALysT and tRNAArgU anneal to form a heterodimer in vitro. The heterodimerisation is prevented by the presence of DNA oligomers complementary to the interacting sequences, in a dose dependent manner. Consistent with the notion of sequestration of tRNAArgU by tRNALysT, while the overexpression of tRNAArgU did not impact the culture growth, that of tRNALysT did. The tRNALysT mediated inhibition of the culture growth was enhanced at a lower temperature. The AGA minigene (decoded by tRNAArgU) mediated toxicity and hybrid phage ({lambda}imm-P22) growth on ssrA (tmRNA) strains was also consistent with the sequestration of tRNAArgU by tRNALysT. Also, we observed tRNA-derived fragments (tRFs) from tRNALysT and tRNAArgU, which too might facilitate tRNAArgU sequestration. Taken together, these observations support a novel regulatory role of the evolutionary conserved complementarities between tRNAs.
]]></description>
<dc:creator><![CDATA[ Sahu, A. K., Dash, A. A., Varshney, U. ]]></dc:creator>
<dc:date>2026-09-04</dc:date>
<dc:identifier>doi:10.64898/2026.09.02.748885</dc:identifier>
<dc:title><![CDATA[Evidence for a regulatory role of the evolutionarily conserved sequence complementarity between tRNAs]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-04</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.08.31.748413v1?rss=1">
<title>
<![CDATA[
EDTP Loss of Function Impairs Longevity and Reproduction 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.08.31.748413v1?rss=1
</link>
<description><![CDATA[
This study presents a comprehensive genetic characterization of DJ694, a viable GAL4 enhancer-trap allele of the age-regulated gene EDTP. EDTP transcript levels are reduced in DJ694, and homozygous flies exhibit reduced reproduction and shortened lifespan in both sexes. The fertility and longevity phenotypes are recessive and can be fully rescued by three independent UAS-EDTP insertions. Expression of UAS-EDTP into animals with wildtype phenotypes does not affect female fertility or lifespan. DJ694 has a jumpy behaviour but it is not detected by a locomotion assay. Like its human homolog, Muscle-specific Inositol Phosphatase (MIP, also known as MTMR14), EDTP is mainly expressed in adult muscles. The structure of the muscle, myofibril, and sarcomere appears normal in homozygous DJ694. DJ694 females have morphologically normal ovaries, implicating a functional rather than structural impairment. We demonstrate that EDTP is required during both development and adulthood to support normal fertility, with expression restricted to either stage alone being insufficient. Although it has been reported that EDTP can influence the accumulation of polyglutamine aggregates, we did not find evidence in its native tissue. Ectopic expression in the eye reduces the amount of aggregates but EDTP overexpression in muscles has no detectable effect on the accumulation or toxicity of two different kinds of polyglutamine aggregates.
]]></description>
<dc:creator><![CDATA[ Lu, X., Barwell, T., Edelman, S., Seroude, L. ]]></dc:creator>
<dc:date>2026-09-04</dc:date>
<dc:identifier>doi:10.64898/2026.08.31.748413</dc:identifier>
<dc:title><![CDATA[EDTP Loss of Function Impairs Longevity and Reproduction]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-04</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.08.31.748193v1?rss=1">
<title>
<![CDATA[
Implication of a rare variant in OPA1 in Cardiac Pathophysiology: From Cristae Remodelling to Contractile Dysfunction 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.08.31.748193v1?rss=1
</link>
<description><![CDATA[
Abstract Optic Atrophy 1 (OPA1), an important inner mitochondrial membrane GTPase, regulates mitochondrial fusion, maintains cristae structure, calcium buffering, cellular bioenergetics, preserves mtDNA and controls apoptosis. Here we examined the role of OPA1 variants in DCM using whole-exome sequencing (WES) of 5 familial and 10 sporadic DCM cases. A rare de novo OPA1 variant, c.563C>T (p.Pro188Leu), was identified in a DCM patient, which is absent in 100 healthy controls as well as in the 1000 Genomes, IndiGenomes and GenomeAsia 100k databases while it showed very low MAF (0.000069) in GnomAD. Structural modelling predicted the variant to be highly deleterious and revealed marked conformational distortion of the mutant protein (RMSD = 3.5 Angstrom). Molecular docking further demonstrated enhanced accessibility of mutant OPA1 to mitochondrial protease OMA1, suggesting increased OPA1 proteolytic processing and a consequent increase in mitochondrial fragmentation. Functional analysis in stable H9C2 cardiomyoblast cells, demonstrated significantly reduced OPA1 protein expression, extensive mitochondrial fragmentation in mutant-OPA1 expressing cells. The mutant protein caused significant reduction in mitochondrial membrane potential, ATP generation, and oxygen consumption rate (OCR), together with elevated cytosolic Calcium and reactive oxygen species (ROS) levels. qRT-PCR analysis further revealed depletion in mtDNA copy number and increased in expression of intrinsic apoptotic markers Caspase3, 9 and Bax/Bcl-2 ratio. The above findings collectively highlighted the significant impact of the OPA1 mutation on mitochondrial dynamics and cellular health, suggesting a significant correlation with the pathogenesis of DCM. Collectively, these findings suggest that OPA1-mediated mitochondrial dysfunction represents a potential therapeutic avenue for the management of DCM.
]]></description>
<dc:creator><![CDATA[ gupta, m., Mukhopadhyay, A., Kumar, A., Mohapatra, B. ]]></dc:creator>
<dc:date>2026-09-04</dc:date>
<dc:identifier>doi:10.64898/2026.08.31.748193</dc:identifier>
<dc:title><![CDATA[Implication of a rare variant in OPA1 in Cardiac Pathophysiology: From Cristae Remodelling to Contractile Dysfunction]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-04</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.08.28.747754v1?rss=1">
<title>
<![CDATA[
The evolutionarily conserved EHMT1/G9a histone methyltransferase family regulates sleep maintenance through ROS homeostasis in insulin-producing cells 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.08.28.747754v1?rss=1
</link>
<description><![CDATA[
Sleep disturbances are a common, still poorly characterized feature of Kleefstra syndrome (KLEFS1), a neurodevelopmental disorder caused by rare variants in the epigenetic regulator EHMT1. The gap in understanding the characteristics and origin of these sleep disturbances poses a major barrier for therapy development. In this cross-species study, we reveal that 70% of individuals with KLEFS1 experience severe sleep maintenance insomnia, marked by fragmented sleep due to frequent night awakenings. Furthermore, common genetic variation at the EHMT1 locus was associated with short sleep and insomnia symptoms in the general population. Drosophila mutants of the EHMT1 orthologue G9a recapitulate these phenotypes, exhibiting reduced and fragmented sleep. We show that G9a is required in insulin-producing cells (IPCs) and the fat body, in the latter during development, to ensure adult sleep integrity. Untargeted metabolomics revealed widespread metabolic dysregulation in G9a mutants, particularly affecting methionine metabolism. Mutants exhibited reduced methionine and elevated methionine sulfoxide (Met-SO), pointing to increased reactive oxygen species (ROS). Redox sensors revealed increased H2O2-dependent oxidation in the larval brain and an elevated glutathione redox potential in IPCs during development but not in adulthood. IPC-specific knockdown of MsrA, the enzyme that reduces Met-SO back to methionine, reproduced sleep fragmentation. Developmental, but not acute, antioxidant treatment fully restored adult sleep consolidation, demonstrating that G9a safeguards sleep via ROS homeostasis in early life. Finally, we show that a Drosophila sleep-restriction paradigm based on human sleep-restriction therapy can override the developmental defects and restore sleep continuity in adulthood. Our findings establish an evolutionarily conserved role for EHMT1/G9a in sleep regulation and provide a mechanistic framework to understand and treat sleep disturbances in KLEFS1.
]]></description>
<dc:creator><![CDATA[ Coll-Tane, M., van Renssen, L. V., Raun, N., Han, J., Ribas-Ros, N., van Reijmersdal, B., Luong, J., Pignato, C., Kampshoff, F., Gong, N. N., Jones, S. G., Pillen, S., Castells-Nobau, A., Mayneris-Perxachs, J., Klein, M., Kayser, M. S., Kleefstra, T., Schenck, A. ]]></dc:creator>
<dc:date>2026-09-03</dc:date>
<dc:identifier>doi:10.64898/2026.08.28.747754</dc:identifier>
<dc:title><![CDATA[The evolutionarily conserved EHMT1/G9a histone methyltransferase family regulates sleep maintenance through ROS homeostasis in insulin-producing cells]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-03</prism:publicationDate>
<prism:section></prism:section>
</item>
</rdf:RDF>
