PLOS Genetics: New Articles

Multi-organ single-cell transcriptomic atlas identifies QrIAA14 as a candidate negative regulator of adventitious root development in Quercus robur

2026-09-01T14:00:00Z

by Wenkai Hui, Jiayue Li, Hao Li, Hongyi Wu, Yi He, Shuangying Yang, Xiong Huang, Hanbo Yang, Gang Chen, Peng Zhu, Xiaohong Chen, Xingcui Xiao, Yu Zhong, Zhenfeng Xu, Fang He

Plant organ development involves coordinated cell fate transitions across multiple tissues, yet the cellular programs underlying organ-specific differentiation in woody plants remain poorly understood, particularly the mechanisms limiting efficient root development during vegetative propagation of oak species. Here, we generated a comprehensive single-cell transcriptomic landscape of leaf, stem, and root tissues of Quercus robur to resolve developmental trajectories at cellular resolution. A total of 41,471 high-quality cells were classified into 30 distinct clusters, enabling the identification of major cell types and organ-specific transcriptional features across three vegetative organs. Pseudotime analyses exhibited the developmental programs related to guard cell differentiation in leaves, vascular formation in stems, and root tissue development. Additionally, combining scRNA-seq, bulk transcriptome profiling, and phytohormone investigations, we identified auxin signaling as an important regulator during adventitious root development process. Notably, QrIAA14-1, an IAA14 homolog, was preferential enrichment in root hair, near-root hair cells and root cap along root developmental trajectories, which was further supported by RT-qPCR and in situ hybridization assays. Furthermore, the overexpression of QrIAA14-1 significantly inhibited oak root elongation, resulting in around 64.46% reduction in adventitious root length compared with control plants, providing mechanistic insight into the limitations of root development in oak. Together, this study provides the first high-resolution single-cell atlas of cellular organization and developmental dynamics across oak vegetative organs and identifies the candidate regulator genes associated with root development, offering new insights into the regulatory mechanisms of woody plant root regeneration and clonal propagation.

Abdominal-B regulates the male seminal fluid transferome and new fecundity factors required for sperm sex peptide binding

2026-09-01T14:00:00Z

by Kathrin Steck, Lina Verbakel, Peter Kerwin, Vladimir Trajanovikj, Katarzyna Kjøge, Jan J. Enghild, Anne C. von Philipsborn

Seminal fluid proteins determine reproductive success in a wide range of animals. In the Drosophila male accessory gland, seminal fluid is mainly produced by two cell types, a majority of main cells and a small number of secondary cells that possess a specialized secretory apparatus with unusually enlarged dense core granule vesicles. Loss of Abdominal-B expression from secondary cells in the enhancer mutant iab-6^cocu disrupts their transcriptional and secretory identity. Consequently, mutant males fail to induce the long-term post-mating response in females, which is characterized by a loss of receptivity and sustained egg laying. Here, we determine how secondary cells shape the seminal transferome and the female response by assessing iab-6^cocu male accessory gland and female mate reproductive tract proteomes. We find downregulation of seminal fluid proteins that constitute a signaling network enabling sperm binding and the sustained action of the key regulator Sex Peptide. We identify two new Sex Peptide network proteins crucial for female fecundity, Cornutus (CG1701) and Hanrej (CG42564). Cornutus is required for mating dependent dense core granule vesicle release, providing a link between the products of these compartments and the female long-term post-mating response. Our data highlights the importance of secondary cell signaling and secretion for overall seminal fluid composition and Sex Peptide network function as well as the interdependence of main and secondary cells and their secretory products, advancing the general understanding of how seminal fluid signaling pathways modulate female physiology, sperm use and offspring production.

Characterization of METTL3/14-mediated m⁶A modification in human transcriptome using Nanopore direct RNA sequencing

2026-09-01T14:00:00Z

by Emily Kurtyan, Andrew J. Stein, Kelly J. Abdalla, Zhangerjiao Yuan, Miten Jain, Fadia Ibrahim

Post-transcriptional RNA modifications modulate diverse aspects of RNA metabolism. N⁶-methyladenosine (m⁶A), one of the most abundant internal RNA modifications, is deposited by the core methyltransferase complex, METTL3 and METTL14. Oxford Nanopore Technologies (ONT) platform permits direct, single RNA molecule sequencing while preserving native modifications. However, without rigorous benchmarking, the accuracy and reproducibility of modification detection remain uncertain. Here, we leveraged ONT to comprehensively profile bona fide m⁶A modifications in cellular RNAs at single-nucleotide resolution by integrating two direct RNA sequencing chemistries (RNA002 and RNA004) with the m6Anet and Dorado modification-detection models. We independently depleted METTL3 and METTL14 in human cells and rigorously validated modification calls through several assays and independent orthogonal methods (GLORI and miCLIP). We find that Dorado detected a higher number of m⁶A events and enabled simultaneous detection of other RNA modifications (5-methylcytosine, pseudouridine, and inosine). Pairing Dorado with an in vitro transcribed, unmodified control under stringent filtering, we provide compelling evidence supporting a global reduction in m⁶A sites and stoichiometry within coding sequences and across genes, particularly in highly modified genes and sites, and at consensus DRACH motifs. We report a differential and complex regulation of modified transcripts, accompanied by a global reduction in poly(A) tail length. Notably, METTL3 and METTL14 depletion produced distinct transcript-specific effects, supporting non-redundant roles within the m⁶A writer complex. Together, our study illustrates a notable advancement of ONT capabilities and establishes a robust transcriptome-wide framework for RNA modification detection, thereby laying the groundwork for exploring the contribution of METTL3/METTL14 to cellular functions and disease.

A drug repurposing screen reveals dopamine signaling as a candidate therapeutic pathway for PIGA-CDG

2026-08-31T14:00:00Z

by Miriam C. Aziz, Jennie Wilson, Clement Y. Chow

PIGA-CDG is a congenital disorder of glycosylation caused by pathogenic partial loss-of-function variants in the PIGA gene. PIGA encodes an enzyme responsible for the catalytic transfer of N-acetylglucosamine to phosphatidylinositol during the first step of glycosylphosphatidylinositol anchor biosynthesis. Loss of this enzyme has a widespread phenotypic impact, but primarily results in neurological symptoms including seizures, intellectual disability, and developmental delay. Currently, treatments are limited and focus on symptom management. We developed an eye model of PIGA-CDG that has a reduced eye size. We screened a library of 98% 1,520 FDA/EMA-approved compounds to find drugs that improved the small eye phenotype. This screen revealed numerous drugs that improved eye size, including those that targeted dopamine signaling and cyclooxygenases. Using pharmacological and genetic approaches, we show that modulating dopamine signaling improves the eye size. Genetic inhibition of dopamine 2 receptor signaling and dopamine reuptake improve both the eye model and neurologically relevant PIGA-CDG phenotypes, including seizures and locomotor deficits. We also pharmacologically and genetically validate cyclooxygenase targeting drugs in the eye model. These findings reveal novel biology underlying PIGA-CDG and point towards candidate therapeutic approaches.

Fungal appressoria as mechanochemical organelles for polyurethane degradation

2026-08-31T14:00:00Z

by Fan Fei, Zhenjie Su, Rui Liu, Rongrong Gao, Chaomin Sun

Polyurethane (PU) is a synthetic polymer characterized by highly stable urethane linkages that hinder biological turnover. Although fungi have been implicated in PU degradation, the molecular mechanisms that couple polymer surface sensing to enzymatic depolymerization remain largely undefined. Here we show that the marine-derived fungus Alternaria alternata FB1 employs a surface-sensing signaling pathway that drives appressorium-mediated degradation of both polyester and polyether PUs. Contact with hydrophobic polymer surfaces rapidly induces melanized appressoria that mechanically penetrate the polymer matrix and promote its oxidative and hydrolytic depolymerization. Integrative transcriptomic analysis and targeted gene disruption identify the mucin-like surface sensor Msb2 as an upstream component of the polyurethane surface-sensing machinery. Loss of Msb2 disrupts MAPK and Ca²⁺ signaling, impairs appressorium differentiation, and reduces expression of degradative enzymes. Biochemical profiling further reveals multiple urethane-hydrolyzing enzymes that expand the known catalytic repertoire for PU bond cleavage. Together, these findings establish a mechanistic framework linking surface recognition, appressorium development, and polymer degradation, providing insight into how fungi transform recalcitrant polyurethane materials.

Convergent latitudinal erosion of circadian systems in a rapidly diversifying order of fishes

2026-08-31T14:00:00Z

by Daniel B. Wright, Yangfan Zhang, Jacob M. Daane

Biological clocks allow organisms to anticipate cyclical environmental changes, yet in high-latitude or deep-sea habitats, the diel cues that entrain these rhythms are often seasonally diminished or absent. Fishes of the order Perciformes have rapidly diversified across these arrhythmic ecosystems, raising the question of whether changes to circadian rhythms and biological clock genetic architecture are a component of their evolutionary success. Here, we used a comparative genomic approach to investigate patterns of core biological clock gene loss across 96 perciform and five outgroup species. We found widespread and lineage-specific loss in core clock genes, particularly in the convergently evolving polar and deep-sea suborders Notothenioidei and Cottoidei. This trend of clock gene loss was significantly amplified with higher-latitude species. To determine if these genomic signatures reflect a functional loss of rhythmicity, we performed metabolic phenotyping on three notothenioid species. We found a consistent lack of circadian metabolic oscillations during the late austral fall across all notothenioids, including the sub-Antarctic sister lineage to the cryonotothenioid adaptive radiation, Eleginops maclovinus. Experimental data across Perciformes, combined with suborder-wide patterns of gene loss, suggest that a release from circadian constraints occurred early in their diversification, potentially facilitating the repeated expansion of these fishes into polar and deep-sea habitats.

Proteobacteria with chemosynthetic potential are highly prevalent in the gills of Hypoplectrus reef fishes

2026-08-28T14:00:00Z

by Sabrin Abdelghany, Martin Helmkampf, Matthew S. Schechter, Iva A. Veseli, Matthieu Leray, A. Murat Eren, Oscar Puebla

Fishes host a diverse microbiome in their gills, but a broad characterization of this microbiome at the metagenomic level is lacking. Here, we apply genome-resolved metagenomics to the gills of the hamlets (Hypoplectrus spp), a group of reef fishes from the Greater Caribbean. The analysis of 353 gill samples from 15 hamlet species collected at eight locations over 13 years revealed a stark contrast between the gill microbiota and reef water microbial communities, indicating a distinct and specific gill microbiome. A total of 70 gill-associated metagenome-assembled genomes (MAGs) were recovered. These MAGs belong to 17 lineages, most of which are novel. They relate to known fish gill pathogens, fish gut microbes, free-living and biofilm-associated taxa, indicating that the gill microbiome was assembled from a collection of distinct eco-evolutionary trajectories. The MAGs harbor diverse metabolic modules, involved notably in nitrogen cycling, antibiotic production and biofilm formation, revealing a highly dynamic microbial ecosystem. One lineage in the Burkholderiaceae family was outstandingly prevalent across fish host species, sampling locations and years. Its genome encoded complete metabolic modules for carbon fixation and sulfur oxidation, indicating chemosynthetic potential. To the best of our knowledge, this is the first line of evidence that fishes may host sulfur-oxidizing chemosynthetic bacteria in their gills. The functional significance of this chemosynthetic potential for the fish host or other members of the gill microbiome remains to be established. The high prevalence of this lineage allowed to build a pangenome. It revealed large-scale geographic structure (western Caribbean, eastern Caribbean and Gulf of Mexico), which parallels the phylogenomic pattern observed in the hamlets. Overall, our findings point to complex fish host-microbe and microbe-microbe eco-evolutionary interactions in the gills that may influence fish physiology, homeostasis and immune response.

Pervasive context-dependent effects in the genetic architecture of complex and quantitative traits revealed by a powerful multiparent mapping population in yeast

2026-08-27T14:00:00Z

by Gareth A. Cromie, Russell S. Lo, Lauren Ames, Trey S. Morgan, Katherine Owens, Anne E. Clark, Martin S. Timour, Julee Ashmead, Michelle Tang, J. Nathan Kutz, Joshua M. Akey, Aimée M. Dudley

The genetic dissection of complex traits remains a major challenge in basic and biomedical research, but is essential for understanding the molecular pathways that shape phenotypic variation and for developing predictive models of trait and disease susceptibility. Here, we leverage a novel multiparent mapping population of budding yeast, CYClones, comprising 9,344 haploid strains derived from eight genetically diverse founders (~270,000 SNVs, ~ 1 per 44 bp, capturing 56% of common variants and 32% of all variants with a minor allele frequency greater than 0.005 in the global population), to identify quantitative trait loci (QTL) and systematically investigate the genetic architecture of growth rates across ten environmental conditions. In total, we identified 349 QTL (ranging from 18 to 49 QTL per growth condition) that explained between 60% and 100% of narrow sense heritability across traits. The high power and resolution of CYClones revealed that growth traits exhibited distinct, condition-specific genetic architectures with extensive allelic heterogeneity, where a QTL was the result of multiple tightly linked causal variants. We also observed pleiotropy among QTL with complex, trait-dependent allele effects that are also consistent with allelic heterogeneity. Genetic complexity varied widely, with some traits showing nearly Mendelian architectures, while others were highly polygenic. Introgressed loci played a prominent role in the landscape of growth rate QTL, including a QTL localized to a 2.4 kb interval in the PCA1 cadmium transporter that explains 72% of variation in cadmium resistance and is largely driven by an introgression, and a non-additive interaction between the GAL3 regulator and introgressed GAL1/7/10 alleles, extending a previously described three-locus GAL-pathway incompatibility to a four-locus interaction. In both cadmium and galactose conditions, we show that allelic variation at a small number of loci stratifies the population into regulatory or physiological subgroups, each with distinct genetic architectures, a specific manifestation of epistasis we term allele-dependent stratification. Collectively, our results provide novel insights into the genetics of growth rates in budding yeast, the architectural features of genetic complexity, and demonstrate that CYClones is a powerful platform for revealing the molecular basis of complex trait variation.

DDI-4 induces a temperature-sensitive exocytotic remodeling during C. elegans spermiogenesis via nsun-2–dependent sphingosine signaling

2026-08-27T14:00:00Z

by Yoshihiro Shimada, Riona Shiraki, Chihiro Ogawa, Nana Kanazawa-Takino, Yukiko Karuo, Kentaro Kawai, Masaharu Hashimoto, Ayaka Yoshida, Arata Honda, Jun Adachi, Jun-Dal Kim, Akiyoshi Fukamizu, Masaaki Omote, Hitoshi Nishimura

Exocytotic sperm remodeling is essential for fertilization, yet whether conserved molecular mechanisms underlie this process across species remains unclear. In Caenorhabditis elegans, membranous organelle fusion (MOF), an exocytotic event cytologically analogous to the mammalian acrosome reaction (ASR), occurs during spermiogenesis and likely contributes to the acquisition of fertilization competence. Here, we identify DDI-4, a benzylamine analog as a small-molecule inducer of both MOF and ASR, revealing a shared sensitivity between these evolutionarily distant systems. DDI-4–induced MOF was selectively impaired in spermatids from males raised at elevated temperatures, whereas conventional protease–induced MOF remained unaffected. Through forward genetics, we isolated the nyg20 mutant, which was specifically defective in DDI-4 responsiveness. Complementation and genetic analyses suggested that the nyg20 phenotype is associated with impaired function of nsun-2, encoding a tRNA methyltransferase, despite the absence of detectable mutations in the nsun-2 coding, intronic, and flanking regions. Consistent with this, an nsun-2 deletion mutant exhibited defects in temperature-sensitive MOF and meiosis. In silico docking analysis further implicated sphingosine kinases (SPHKs) as candidate targets of DDI-4; indeed, loss of sphk-1 phenocopied the nsun-2 mutant. Moreover, we tested sphingosine (SPH) and its analog FTY720 as MOF activators, using mutants lacking sphk-1 or spin-4, which encodes a transporter of phosphorylated SPH. Intriguingly, DDI-4 and SPH activated MOF in an SPHK-1–dependent but SPIN-4–independent manner, whereas FTY720 required both SPHK-1 and SPIN-4 for MOF activation. Because DDI-4 lacks hydroxyl groups that SPHKs typically phosphorylate, these findings suggest that SPHK-1 may function not only as a kinase but also as a scaffold for downstream signaling. Together, our results reveal a temperature-sensitive, NSUN-2–dependent SPH-mediated signaling axis that regulates organelle exocytosis during spermiogenesis and suggest an evolutionarily conserved mechanism underlying fertilization competence.

Correction: The Janus-faced Nature of miR-22 in Hematopoiesis: Is It an Oncogenic Tumor Suppressor or Rather a Tumor-Suppressive Oncogene?

2026-08-25T14:00:00Z

by The PLOS Genetics Editors

An ancient alpharetrovirus lineage in bats: Evolutionary insights and possible roles in reproduction

2026-08-25T14:00:00Z

by Emma F. Harding, Zhaobo Zhang, Charles Reuben De Souza, Jose Gabriel Nino Barreat, Aris Katzourakis

Alpharetroviruses are an important group of pathogens that are known for causing leukemias and tumors and were historically considered to be restricted to avian hosts. The identification of alpharetrovirus-like envelopes in bat genomes has hinted at a potentially wider host range, although their relations to modern alpharetroviruses and distribution remains unclear. Through a paleovirological screening of 818 vertebrate genomes we identified CHIRalphaEnv, a lineage that belongs firmly within alpharetroviruses, and emerged from a cross-class transmission from saurian hosts. We determine that CHIRalphaEnv envelope genes have been co-opted across bats on eight separate occasions between 43.8 and 18.9 million years ago and are preserved in most bat genomes screened. CHIRalphaEnv elements encode full-length envelope proteins and have been maintained under purifying selection, demonstrating multiple instances of exaptation by their bat hosts and a likely ubiquitous function. We observe high expression levels of CHIRalphaEnv envelopes in endometrium tissue from Carollia perspicillata, suggesting an involvement in reproductive function. We find CHIRalphaEnv sequence relatives in multiple mammalian clades (Afrotherians, rodents and bats), expanding the host range and extending origins of alpharetroviruses beyond 43 million years. We also propose the first mammalian co-opted Endogenous retrovirus (ERV) derived from an Alpharetrovirus envelope and explore the convergent functional recruitment of CHIRalphaEnv in hemochorial placentation in bats, elephant shrews and spiny mice. These findings highlight alpharetroviruses as a previously underappreciated source of functional exaptation in mammals.

Replication-transcription collisions impose DNA strand-specific constraints on gene length in bacteria

2026-08-24T14:00:00Z

by Anjali Variyar, Samhitha Patil, Jebin Babu, Akanksha Bhat, T. Sabari Sankar

Gene length is a peculiar genomic feature that exhibits minimal variation within domains of life, suggesting universal underlying constraints. The length of a gene is primarily influenced by its function, expression level, and mutation risk. Interestingly, many of these factors vary depending on whether the gene is located on the leading or lagging strand of DNA replication. Studies in bacterial species E. coli and B. subtilis have shown that genes tend to be shorter on the lagging strand, potentially reflecting selection to minimize head-on encounters between the replication and transcription machinery. However, the universality of strand-specific constraints on gene length and the evolutionary basis remain unexplored. Here, using comparative genomics, we analyzed gene lengths in the bacterial domain and revealed a non-neutral distribution of gene lengths across leading and lagging strands. Genes and operons are consistently shorter on the lagging strand, irrespective of essentiality or functionality. The length restriction was more pronounced in bacterial species with a dual DNA polymerase mode of replication, which may experience severe head-on collisions between replication and transcription. Remarkably, we found that with increasing length of transcription units, substitution rates increased in the promoters on the lagging strand rather than the coding sequences, revealing a length-dependent and lagging strand-specific cis-regulatory mutational susceptibility. Together, we uncovered a pervasive selection pressure that optimizes gene lengths in a DNA strand-specific manner across bacteria to preserve the genetic integrity of promoters.

Hippo signaling regulates cuticle pigmentation and dopamine metabolism in Drosophila

2026-08-21T14:00:00Z

by Shelley B. Gibson, Samantha L. Deal, Ye-Jin Park, Bo Sun, Yanyan Qi, Jung-Wan Mok, Hyung-Lok Chung, Hongjie Li, Shinya Yamamoto

Pigmentation plays multiple important roles in development, physiology and evolution. Melanization of the insect cuticle requires dopamine as a precursor of melanin and involves key enzymes in dopamine biosynthesis including Tyrosine hydroxylase (TH) and Dopa decarboxylase (Ddc). Some studies have hinted that disruption of the evolutionarily conserved Hippo signaling pathway, which has been primarily studied in the context of tissue growth, may lead to changes in cuticle pigmentation in the fruit fly Drosophila melanogaster. However, to our knowledge, there have not been any systematic investigations into their potential mechanistic links. In this study, we identified that all genes that comprise the canonical Hippo signaling pathway [hippo (hpo), salvador (sav), mats, warts (wts), yorkie (yki) and scalloped (sd)] are involved in cuticle pigmentation in the fly notum based on tissue-specific gene knock-down/out experiments and epistatic analysis. Despite the notable divergence of pigmentation mechanisms between invertebrates and vertebrates, these phenotypes can often be rescued by the human orthologs of corresponding fly genes. While we find that manipulation of Hippo signaling in dopaminergic neurons does not affect global dopamine levels in the fly brain, developmental inhibition of this pathway can increase dopamine levels in the fly head, indicating that the mechanism by which dopamine levels are regulated in the nervous system is distinct from that in epithelial cells. Through single nuclei RNA sequencing of the developing fly nota and subsequent functional studies of differentially expressed genes that are altered upon inhibition of Hippo signaling, we found many genes that contribute to cuticle pigmentation downstream of Hippo signaling. We conclude that regulation of cuticle pigmentation by canonical Hippo signaling acts through multiple downstream genes rather than directly through TH and Ddc. We also propose that the Drosophila melanogaster cuticle may serve as a useful platform to identify previously uncharacterized mediators of Hippo signaling as well as an in vivo experimental system to test the functionality of rare genetic variants found in human Hippo signaling orthologs associated with a variety of diseases.

Telomeric amplicons of SUL1 and Y’ in yeast are generated by microhomology-mediated break induced replication occurring in cis

2026-08-20T14:00:00Z

by Bonita J. Brewer, Rebecca Martin, Elizabeth Ramage, Celia Payen, Sara C. Di Rienzi, Yang Zhao, Kelsey M. Van Sickle, Jocelyn Verhey, Miranda Zalusky, Danny E. Miller, Giang T. Ong, Jamie L. McKee, Gina M. Alvino, Maitreya J. Dunham, M. K. Raghuraman

Gene amplification is a potent driver of evolution and is thought to contribute to genetic diseases, including cancer. The yeast Saccharomyces cerevisiae is a powerful organism for understanding amplification mechanisms. When yeast is grown long term in sulfate-limiting chemostats, amplification of the gene that encodes the primary sulfate transporter, SUL1, is a common outcome. Here we describe a form of SUL1 amplification in which multiple copies of the right terminal region of chromosome II are appended in tandem to a native telomere. We find this form of amplicon when we delete the origin of replication next to SUL1 or delete a variety of genes involved in DNA metabolism. It is the only form of amplification found in a yku70Δ mutant suggesting that telomeres are involved. We propose that these terminal addition events occur when a destabilized 3’ G_1-3T telomeric sequence invades a short (~7 bp) internal telomere sequence (ITS) to begin a form of microhomology-mediated break-induced replication (mmBIR) that has been documented in type-I survivors of telomerase mutants. In addition to amplification of the right end of chromosome II we also find that telomeres containing the sub-telomeric repeat Y’ experience similar tandem amplification events and show that their formation is reduced in a pol32Δ mutant, a gene involved in mmBIR. Within individual amplicons the expanded ITSs and Y’s are nearly identical, suggesting that the multiple copies of the amplified region are generated in a single mmBIR event that we describe as pseudo-rolling circle mmBIR. A similar amplification event at the P-telomere of human chromosome 18 has four copies of a ~ 54 kb region separated by ITSs of nearly identical size. This finding suggests that these additional copies of the terminal fragment of human chromosome 18 arose by the same pseudo-rolling circle mechanism, perhaps during a period of telomeric stress.

Neuronal Nrf/SKN-1B controls a sexually dimorphic neuroendocrine pathway for C. elegans exploratory behaviour

2026-08-13T14:00:00Z

by Noviann McLean, Minaxi S. Gami, Nathan Dennis, Yasir Malik, Justin De Araujo, James Evans, Lydia Bennett, Marina Ezcurra, Jennifer M. A. Tullet

The SKN-1/Nrf transcription factor family is integral to metabolic homeostasis. There are three SKN-1 isoforms in Caenorhabditis elegans, each with different functions. One of these, SKN-1B, is expressed specifically in neurons and controls hermaphrodite behaviour in response to food. In a laboratory environment C. elegans hermaphrodites must allocate energy efficiently between exploratory food-seeking behaviour, reproduction, and survival, whereas males have to balance both food-seeking with mate-seeking exploratory behaviours. Here, we evaluate the role of SKN-1B in male behaviour and show that SKN-1B acts in a sexually dimorphic manner to control exploratory behaviour, mitochondrial morphology, and mitochondrial function. Moreover, we show that SKN-1B is expressed in a sexually dimorphic pattern, and that SKN-1B influences gene expression on a much broader scale in males compared to hermaphrodites. This analysis identified a neuronal signalling pathway, specifically in males between SKN-1B, the TGF-β ligand DAF-7 and the chemosensory regulator ODR-10, and that this pathway contributes to increased exploratory behaviour in skn-1b mutant males. Taken together our findings identify SKN-1B as a sex-specific neuronal switch to control food searching and mating behaviours. Sexual dimorphism is essential for optimizing survival and reproductive success and our findings establish SKN-1B as a regulator of sex-specific behavioural and metabolic traits. This work provides new insights into neuronal regulation of metabolism and behaviour, with implications for sex-specific physiological adaptations in other species.

New biologically relevant resistance to bacterial wilt in heat-stressed tomato revealed by two-reference Genome Wide Association

2026-08-13T14:00:00Z

by Adrien Belny, Henri Desaint, Mylène Rigal, Sébastien Carrère, Jérôme Gouzy, Gregori Bonnet, Céline Labourey, Elise Albert, Laurent Grivet, Fabrice Roux, Fabienne Vailleau, Tristan Mary-Huard, Richard Berthomé

Ongoing climate change is driving unprecedented environmental fluctuations, with extreme events predicted to increase in frequency, intensity and duration. Among climatic parameters, temperature is expected to fluctuate the most by the end of the century and its elevation has already demonstrated to pose a major challenge to plant health. In this context, understanding how temperature modulates plant-pathogen interactions and their underlying genetic architecture is critical. Bacterial wilt, caused by strains of the Ralstonia solanacearum species complex, is a devastating disease affecting many plant species. Genetic resistance remains the most effective control strategy. In tomato, resistance is quantitative and mostly relies on quantitative trait loci (QTLs) bwr-6 and bwr-12. However, as in other crops, high temperature and humidity can compromise this resistance in commercial tomato cultivars. We investigated temperature-dependent quantitative disease resistance (QDR) using a panel of 189 wild tomato accessions, predominantly Solanum pimpinellifolium, representing genetic diversity from contrasting ecological conditions. Disease progression was monitored from three to ten days post-inoculation at 28 °C and 32 °C, using a time-course phenotyping approach. Genome-wide association (GWA) analyses were performed, based on daily symptom scores and two reference genomes, to account for structural variations and improve QTL detection. This strategy identified 44 candidate genes and revealed a temporally dynamic genetic architecture of the plant response. Strikingly, no candidate genes were shared between temperatures, supporting distinct genetic determinants under different temperature conditions. Many candidate genes were expressed in roots and belong to gene families involved in plant immunity, with two candidates co-localizing with bwr-6 and bwr-12, whose causal genes remain unknown. Altogether, our findings demonstrate that resistance to bacterial wilt in wild tomato is flexible, environment-dependent, and temporally dynamic, highlighting the importance of integrating environmental context and genomic diversity to better understand plant-pathogen interactions.

Genomic constraint and hypervariability correlate with fitness effects in elite tetraploid potato breeding material

2026-08-11T14:00:00Z

by Trine Aalborg, Zihui Ding, Yaoyao Wu, Elsa Sverrisdóttir, Kåre Lehmann Nielsen, Guillaume P. Ramstein

Tetraploid potato is the most important vegetable food crop in the world. However, genetic gains from modern breeding efforts have been limited due to tetrasomic inheritance, the accumulation of deleterious mutations during domestication, and subsequent clonal propagation during modern breeding. In this study, we analyzed previously identified evolutionarily constrained genomic regions in the potato genome relative to a breeding panel of tetraploid potato clones derived from elite cultivars (the MASPOT panel). We demonstrate a significant association between derived allele frequency (DAF) and both positive (constrained) and negative (excess of substitutions relative to neutrality, i.e., hypervariable) nucleotide conservation scores (GERP scores) in the breeding panel, indicating that negative GERP scores can annotate sites affected by positive selection or other non-neutral processes affecting population allele frequency. The deep phylogeny approach can be leveraged to alleviate inbreeding in potatoes through the qualification of causative alleles in tetraploids, offering a valuable resource for potato genetic improvement by molecular breeding. Estimates of genetic load within the tetraploid clones reveal that heterozygous loads vastly exceed homozygous loads for deleterious alleles, consistent with masking of recessive mutations. Deleterious load was significantly correlated with several trait phenotypes but did not improve prediction accuracy of any traits in the tetraploid panel. This could be due to the increased complexity of tetrasomic inheritance, including more effective load complementation, and/or a higher proportion of heterozygosity in tetraploid compared to diploid potato. Intriguingly, the hypervariable load correlated significantly with several phenotypes and improved genomic prediction accuracy of yield by 5% relative to a negative control (permuted loads). This indicates that the inferred hypervariable sites from Solanaceae evolutionary information may contain genetic information relevant for breeding, and that, in contrast to current practice, it is relevant to include and further explore sites with negative GERP scores in general.

Lysine deficiency within a conserved lysine desert is critical for EEL-1/HUWE1 to support ubiquitin proteasome system function

2026-08-10T14:00:00Z

by Katherine S. Yanagi, Brenda J. Chen, Sheikh Omar Kunjo, Irini Topalidou, Nicolas Lehrbach

The ubiquitin proteasome system (UPS) is the primary mechanism for targeted protein degradation in eukaryotic cells. Dysfunction of this system is a driver of human disease and a hallmark of aging and late-onset neurodegenerative disorders. Understanding the mechanisms that ensure robust protein turnover may provide new avenues for treatment in these contexts. E3 ubiquitin ligases play critical roles in supplying ubiquitinated substrates to the proteasome, with HUWE1 being an enormous, versatile, and highly conserved member of this family. Here, we show that the C. elegans HUWE1 ortholog EEL-1 contributes to robust protein turnover, particularly during conditions that challenge the proteolytic capacity of the proteasome. We demonstrate that the ability of EEL-1/HUWE1 to safeguard protein turnover requires the HECT-type ubiquitin ligase activity, supporting a model in which EEL-1 ensures degradation via substrate ubiquitination. EEL-1 contains extensive lysine-deficient regions, found at conserved locations in its substrate-binding arena. Through unbiased mutagenesis screening and precise engineering of the EEL-1 protein, we uncover that introducing lysine residues into these regions is detrimental to UPS function and to animal physiology. Together, our findings indicate a central and evolutionarily ancient role for EEL-1/HUWE1 in maintaining optimal UPS function and support targeting this E3 for therapeutic manipulation.

Integrating short-read and long-read single-cell transcriptomics of pig pituitary reveals mechanisms of high-altitude hypoxia adaptation

2026-08-10T14:00:00Z

by Hai Li, Xudong Wu, Hailong Huo, Xia Zhang, Yiming Guo, Wan Lin, Feidi Wen, Zhijun Zhao, Guiying Zhao, Jinlong Huo

Acting as the central endocrine hub, the pituitary gland is closely related to the mechanism of adaptation to high-altitude hypoxia. Here, by integratively combining long-read (Oxford Nanopore) and short-read (Illumina) single-cell sequencing approaches, we profiled pituitaries from Diqing Tibetan pigs, inhabiting high-altitude environments (3,200 m) and Diannan small-ear pigs from low-altitude regions (500 m), thereby generating a full-length single-cell atlas, which in turn enabled the identification of molecular mechanisms potentially underlying adaptation to high-altitude hypoxia stress. Systematically delineating pituitary structure and transcriptional dynamics, we profiled 27,339 single cells encompassing 28,932 expressed genes. Leveraging unsupervised clustering coupled with marker-based annotation, we identified ten major cell types. Expression profiling of 20 canonical marker genes revealed pronounced cell-type-specific expression patterns, ten of which were independently validated by immunofluorescence, thus substantiating the accuracy of cell-type annotation. Gene-ontology enrichment analysis further suggested that upregulated genes were predominantly involved in oxidative metabolism and energy production, whereas downregulated genes were significantly associated with protein biosynthesis and translation processes, indicating a functional reprogramming of metabolic pathways. Moreover, comparative analyses between breeds and cell–cell communication analyses highlighted pathway shifts, including broad upregulation of the collagen family and four ligand–receptor pairs that may mediate pituitary intercellular coordination. In parallel, transcription-factor activity analysis nominated several regulators, including EBF3, DBX2, and TCF21, which may collectively contribute to altitude-associated adaptation. Finally, integrating long-read sequencing data revealed widespread transcript isoform diversity, with ~28% novel annotations, indicating considerable isoform complexity in pigs. Our findings delineate cellular heterogeneity, inferred intercellular communication networks, and transcript-isoform diversity in the porcine pituitary, thereby providing a cell-resolved resource for understanding pituitary features associated with high-altitude environments.

Social isolation upregulates takeout expression in female Drosophila melanogaster to promote sucrose preference

2026-08-10T14:00:00Z

by Elisabeth A. Tawa, Lisa Schneper, Katherine I. Cho, Mindy Sim, Eve Schoeffler, Daniel A. Notterman

Previous research suggests that social isolation induces changes in gene expression that encode a starvation-like brain state and reduce sleep. However, the extent to which social isolation alters behaviors via sex-specific brain changes is unclear. Here, we use Drosophila melanogaster to explore sex differences in isolation-induced behavioral and transcriptomic changes. Male and female adult flies were isolated for seven days, and multiple behavioral sex-based differences were identified through tests of activity, motivation, aggression, and sugar preference. RNA-seq analysis also identified several candidate genes that were associated with sex differences in isolation-induced behavioral changes. Takeout (to) expression and sucrose selection were upregulated exclusively in females following social isolation. Following to knockdown in to-expressing cells, sucrose preference decreased in socially isolated females but increased in males. Overall, our results suggest that manipulating to expression influences sucrose choice in opposite directions between females and males following social isolation. It is possible that isolation-induced to overexpression in non-neuronal cells in the female head could contribute to sex differences in this behavior.

Correction: Bendless is essential for PINK1-Park mediated Mitofusin degradation under mitochondrial stress caused by loss of LRPPRC

2026-08-05T14:00:00Z

by Rajit Narayanan Cheramangalam, Tarana Anand, Priyanka Pandey, Deepa Balasubramanian, Reshmi Varghese, Neha Singhal, Sonal Nagarkar Jaiswal, Manish Jaiswal

The rights and wrongs of rescaling in population genetics simulations

2026-08-05T14:00:00Z

by Parul Johri, Fanny Pouyet, Brian Charlesworth

Computer simulations of complex population genetic models are an essential tool for making sense of the large-scale datasets of multiple genome sequences from a single species that are becoming increasingly available. A widely used approach for reducing computing time is to simulate populations that are much smaller than the natural populations that they are intended to represent, by using parameters such as selection coefficients and mutation rates whose products with the population size correspond to those of the natural populations. This approach has come to be known as rescaling, and is justified by the theory of the genetics of finite populations. Recently, however, there have been criticisms of this practice, which have brought to light situations in which it can lead to erroneous conclusions. This paper reviews the theoretical basis for rescaling, and relates it to current practice in population genetics simulations. It shows that some population genetic statistics are scaleable while others are not. Additionally, it shows that there are likely to be problems with rescaling when simulating large chromosomal regions, due to the non-linear relation between the physical distance between a pair of separate nucleotide sites and the frequency of recombination between them. Other difficulties with rescaling can arise in connection with simulations of selection on complex traits, and with populations that reproduce partly by self-fertilization or asexual reproduction. A number of recommendations are made for good practice in relation to rescaling.

Glial cell toxicity in a Drosophila C9orf72 neurodegeneration model

2026-08-05T14:00:00Z

by Isabel Hubbard, Josh Dubnau

The most common genetic cause of both familial amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is an expanded G₄C₂ repeat in the first intron of the gene C9orf72. The C9orf72 repeat expansion is bidirectionally transcribed into sense and anti-sense RNA foci, and also produces dipeptide repeats (DPRs) via a non-canonical translation mechanism known as repeat-associated (RAN) translation. Each of these components of the G₄C₂ repeat expansion cause neurodegenerative effects in animal models when expressed in neurons, but impacts from glial expression are more poorly understood. Here, we use glial cell type-specific expression of individual DPRs, of RNA repeat-only, or of the G₄C₂ repeat, that produces both DPRs and RNA repeats, to systematically investigate glial toxicity of each component. We find that as with neurons, the GR and G₄C₂ transgenes produce the highest degree of toxicity when expressed in glia. Each of these transgenes are capable to produce the GR DPR, which also is the most toxic factor in neurons. We demonstrate that both the GR and G₄C₂ transgenes cause activation of mdg4, an endogenous retrovirus (ERV). Such ERV expression is a hallmark of TDP-43 dysfunction that is commonly observed in C9orf72 patients. We find that glial expression of either the GR or the G₄C₂ transgene is toxic to glial cells, but such expression does not cause loss nearby neurons. However, blocking apoptotic signaling within glia that express either GR or G₄C₂ via expression of the p35 caspase inhibitor further exacerbates effects on lifespan and ablating such glia via expression of the proapoptotic reaper gene partially ameliorates these effects. Together, these results indicate that expression of toxic C9orf72 components in glia produces deleterious effects on lifespan, though potentially through different mechanisms than seen in TDP-43 models of ALS/FTD.

Gene network analysis predicts the primary regulators of ABA-dependent transcriptional activation and repression in Populus roots

2026-08-04T14:00:00Z

by David Cohen, Maira De Freitas Pereira, Iva Pavlović, Ondrej Novák, Marie-Béatrice Bogeat-Triboulot, Sarah Jane Cookson, Irène Hummel

Abscisic acid (ABA) acts as a key signalling molecule that mediates plant responses to environmental cues as well as plant growth and development. Stress-induced and developmental changes in ABA content trigger a myriad of post-transcriptional and transcriptional events. Yet, ABA-dependent transcriptional responses are context dependent, and their temporal dynamics in roots under non-stress conditions remain poorly resolved. In this study, we characterised the hallmarks of ABA signalling and responses in the poplar root transcriptome (Populus nigra L.). We disturbed ABA homeostasis by exogenous ABA treatments, and we combined time-resolved transcriptomics with unsupervised gene network analysis to identify ABA-activated and ABA-inactivated gene co-expression modules. Considering the temporal dynamics of transcriptional events, we predicted the primary targets of the ABA signal, characterised early responding ABA-dependent processes, identified hub genes and revealed their putative functional links. We demonstrated that the properties of a master ABA-activated module induced by exogenous treatments were preserved in the transcriptome response to osmotic stress, revealing a core gene set of ABA-dependent stress responses. Our work sheds light on ABA repression of gene expression, the reprogramming of metabolism and the leaf-senescence pathway. Based on current functional knowledge and phylogenetic information, including poplar-specific features, we proposed a working model of ABA action on root transcriptome in poplar that integrates master genes, key responsive processes, and their putative regulatory architecture.

Correction: Meta-evolutionary exome analysis identifies novel type 2 diabetes mellitus genes in the UK Biobank and All of Us

2026-08-03T14:00:00Z

by The PLOS Genetics Staff

Disruption of small RNAs and mechanistic variation in Segregation Distorter: A sperm-killing drive system in Drosophila melanogaster

2026-08-03T14:00:00Z

by Logan T. Edvalson, Xiaolu Wei, Ching-Ho Chang, Amanda M. Larracuente

Meiotic drivers achieve biased transmission to the next generation, often at the expense of their host. Drive is widespread and can shape the evolution of proteins, chromosome structure, and karyotypes. The sperm killer Segregation Distorter (SD) in Drosophila melanogaster is a well-studied driver but like most complex drivers, its mechanism remains elusive. SD is a multigene complex frequently associated with chromosomal inversions where the main driver locus, a truncated duplication of the gene RanGAP, kills wild-type sperm containing a satellite DNA called Responder (Rsp). Small RNAs are frequently implicated in the mechanisms of sperm killers, and we recently showed that Rsp is a source of small RNAs. Here we study the transcriptomes of two SD haplotypes and our results link Rsp expression and/or RNAs to drive. We found that Rsp-derived small RNAs are underrepresented in driving testes of only one of the SD haplotypes. We show that over-expressing Rsp is sufficient to reduce drive strength in the haplotype with downregulated Rsp but not the other. We therefore shed light on the mechanism of SD by making a connection between the target and the drive phenotype. Additionally, our data imply that different haplotypes of complex drivers, like SD, can vary in their mechanism.

Correction: Complexin in ivermectin resistance in body lice

2026-07-30T14:00:00Z

by The PLOS Genetics Editors

Matrix Metalloprotease 1 (Mmp1) promotes cell fate change for epithelial-to-epithelial transition during regeneration after radiation damage in Drosophila

2026-07-30T14:00:00Z

by Michael Shiferaw, Lauren Orr, Korneel Hens, Tin Tin Su

Ionizing radiation (IR) is used to treat cancer, but therapeutic failure occurs when surviving cancer cells change fate and regenerate tumors through acquired stem cell-like properties. While transcriptional mechanisms underlying cell fate plasticity have been characterized, the cellular processes enabling cell movement during tissue regeneration remain unclear. We reported previously that hinge cells of the Drosophila larval wing disc convert to pouch fate and translocate to help regenerate the pouch that suffers from more IR-induced apoptosis. We report here that IR increases the expression of extracellular proteins in the hinge, including secreted proteases and cell adhesion modulators. Functional validation using RNA interference revealed that secreted Matrix Metalloprotease 1 (Mmp1) and the related secreted protease homolog Scarface (Scaf) are required in hinge cells for IR-induced cell fate conversion and translocation. IR, we found, induces Mmp1 and scaf transcripts in hinge cells via cell-autonomous JNK signaling. Overexpression of Mmp1 specifically in the hinge was sufficient to elevate Mmp1 protein levels throughout the disc and induced cell fate change of both hinge and non-hinge cells but only in the context of irradiation. Confocal imaging in a time course demonstrated that cells undergoing fate conversion remain within the epithelial layer with little evidence for delamination or epithelial-mesenchymal transition (EMT). We propose that remodeling of the extracellular environment is a critical mechanism that enables cellular reorganization during tissue regeneration. Mmp enzymes are important for cancer biology because of their role in ECM remodeling, extracellular signaling, and EMT. Our findings demonstrate for the first time that Mmp1 is necessary and sufficient for one epithelial cell type to switch to another epithelial cell type after radiation damage. These results provide a mechanistic basis for radiation therapy-induced cell fate plasticity.

Recurrent evolution of cryptic triploids in cultivated enset increases yield

2026-07-24T14:00:00Z

by Yann Dussert, James S. Borrell, Jonathan Stocks, Harriet V. Hunt, Oliver W. White, Paul Wilkin, Richard Buggs, Lucie Büchi, Sebsebe Demissew, Feleke Woldeyes, Ilia J. Leitch, Wendawek M. Abebe, Richard A. Nichols

The high incidence of polyploidy in crops could be explained if domestication involved the selection of polyploids (cytotypes with more than two sets of chromosomes). Ancestral horticulture could have targeted desirable traits including yield, robustness to stress or disease, rather than requiring knowledge of polyploidy itself. We find evidence for this process underway in enset (Ensete ventricosum, Musaceae), a highly resilient crop constituting the main staple for over 20 million people in Ethiopia, which is clonally propagated and cultivated for its starch-rich corm and pseudostem. Prior to this study, enset was thought to be exclusively diploid (2n = 2x = 18). Using a newly-assembled chromosome-scale reference genome and sequence data from 723 wild and domesticated enset individuals from southwestern Ethiopia, we demonstrate that around 20% of cultivated enset clones are triploid. We show that triploidy has arisen multiple times independently, that the triploid lineages have been given distinct landrace names, and planted disproportionately frequently. Enset triploid clones also have a higher pseudostem volume than diploids on average. As well as providing evidence for enduring selection on triploids, our results reveal valuable genetic diversity captured by these triploid lines. They represent key resources for scientifically directed breeding of this major crop in the Ethiopian agrosystem, and could improve food security in Sub-Saharan Africa.

Partitioning of the truncated insulin receptor DAF-2B between homodimers and heterodimers influences insulin signaling in C. elegans

2026-07-23T14:00:00Z

by Bryan A. Martinez, Anne M. Stene, Jonathan I. Hauser, Karla J. Opperman, Jonathan N. Sachs, Anthony R. Braun, Matthew S. Gill

Insulin / insulin-like growth factor signaling (IIS) in C. elegans is mediated by the DAF-2 receptor and insulin-like peptides (ILP) that can act as agonists or antagonists. DAF-2 signaling is also affected by DAF-2B, a truncated, non-signaling, secreted isoform of DAF-2 that acts as a decoy receptor by sequestering ILPs. In this study, we performed a forward genetic screen for modifiers of DAF-2B protein expression and identified a mutation in unc-31 that increased DAF-2B. UNC-31 is involved in dense core vesicle docking and is required for neuropeptide secretion, including ILPs. As a result, unc-31 mutants constitutively enter the dauer larval stage and are long-lived due to reduced IIS. We find that increased nervous system DAF-2B accumulation is associated with reduced agonist ILP availability, in both unc-31 mutants and wild type worms. Using auxin-induced degradation (AID) and fluorescence lifetime imaging microscopy-Förster resonance energy transfer (FLIM-FRET), we find that a significant fraction of nervous system DAF-2B is in the form of a heterodimeric complex with a full-length DAF-2 receptor isoform, representing a new class of DAF-2 hybrid receptor. In unc-31 mutants, DAF-2B also undergoes endocytosis in neurons in an AP2-dependent manner and genetic manipulation of daf-2b in the unc-31 mutant suggests that DAF-2B homodimers may function to reinforce a reduced insulin signaling state by clearing agonist ILPs from the extracellular space. These findings indicate that DAF-2B not only forms homodimers, but also hybrid receptors with full-length DAF-2, to regulate the activity of the large and diverse family of ILPs in C. elegans.

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A drug repurposing screen reveals dopamine signaling as a candidate therapeutic pathway for PIGA-CDG

Fungal appressoria as mechanochemical organelles for polyurethane degradation

Convergent latitudinal erosion of circadian systems in a rapidly diversifying order of fishes

Proteobacteria with chemosynthetic potential are highly prevalent in the gills of Hypoplectrus reef fishes

Pervasive context-dependent effects in the genetic architecture of complex and quantitative traits revealed by a powerful multiparent mapping population in yeast

DDI-4 induces a temperature-sensitive exocytotic remodeling during C. elegans spermiogenesis via nsun-2–dependent sphingosine signaling

Correction: The Janus-faced Nature of miR-22 in Hematopoiesis: Is It an Oncogenic Tumor Suppressor or Rather a Tumor-Suppressive Oncogene?

An ancient alpharetrovirus lineage in bats: Evolutionary insights and possible roles in reproduction

Replication-transcription collisions impose DNA strand-specific constraints on gene length in bacteria

Hippo signaling regulates cuticle pigmentation and dopamine metabolism in Drosophila

Telomeric amplicons of SUL1 and Y’ in yeast are generated by microhomology-mediated break induced replication occurring in cis

Neuronal Nrf/SKN-1B controls a sexually dimorphic neuroendocrine pathway for C. elegans exploratory behaviour

New biologically relevant resistance to bacterial wilt in heat-stressed tomato revealed by two-reference Genome Wide Association

Genomic constraint and hypervariability correlate with fitness effects in elite tetraploid potato breeding material

Lysine deficiency within a conserved lysine desert is critical for EEL-1/HUWE1 to support ubiquitin proteasome system function

Integrating short-read and long-read single-cell transcriptomics of pig pituitary reveals mechanisms of high-altitude hypoxia adaptation

Social isolation upregulates takeout expression in female Drosophila melanogaster to promote sucrose preference

Correction: Bendless is essential for PINK1-Park mediated Mitofusin degradation under mitochondrial stress caused by loss of LRPPRC

The rights and wrongs of rescaling in population genetics simulations

Glial cell toxicity in a Drosophila C9orf72 neurodegeneration model

Gene network analysis predicts the primary regulators of ABA-dependent transcriptional activation and repression in Populus roots

Correction: Meta-evolutionary exome analysis identifies novel type 2 diabetes mellitus genes in the UK Biobank and All of Us

Disruption of small RNAs and mechanistic variation in Segregation Distorter: A sperm-killing drive system in Drosophila melanogaster

Correction: Complexin in ivermectin resistance in body lice

Matrix Metalloprotease 1 (Mmp1) promotes cell fate change for epithelial-to-epithelial transition during regeneration after radiation damage in Drosophila

Recurrent evolution of cryptic triploids in cultivated enset increases yield

Partitioning of the truncated insulin receptor DAF-2B between homodimers and heterodimers influences insulin signaling in C. elegans

Characterization of METTL3/14-mediated m⁶A modification in human transcriptome using Nanopore direct RNA sequencing