Biology subjects

Tay, R. J.

Publications and source records attributed to Tay, R. J..

5 recordsLinked to original sources

bioRxiv2026

Gene duplication of SNAPC1 generates transcription factors for snRNAs and sex-specific piRNAs

Piwi-interacting RNAs (piRNAs) are small non-coding RNAs essential for transposon silencing and germline integrity across metazoans. In many species, piRNA expression is sexually dimorphic, yet the molecular mechanisms underlying this sex specificity remain poorly understood. In Caenorhabditis elegans, sexually dimorphic piRNA expression is regulated at the transcriptional level. We previously identified SNPC-1.3, a paralog of the small nuclear RNA (snRNA) activating protein complex (SNAPc/SNPC) subunit SNAPC1, as a male-specific piRNA transcription factor. However, the factors governing female piRNA expression remained elusive. Here, we identify SNPC-1.2, a second SNPC-1 paralog, as a female-specific piRNA transcription factor. SNPC-1.2 interacts with the core piRNA transcriptional machinery, binds female piRNA loci, is required for female piRNA expression, and promotes hermaphrodite fertility. In contrast, a third paralog, SNPC-1.1, retains the ancestral SNAPc function in snRNA transcription and is dispensable for piRNA biogenesis. Together, these findings reveal how gene duplication and functional specialization within the snpc-1 gene family generate specificity factors that direct the core SNAP complex to distinct genomic targets, providing a molecular mechanism for sexually dimorphic piRNA expression while maintaining canonical snRNA transcription.

molecular biology↗

bioRxiv2025

Establishment of a Congenic Strain for the Oyster mushroom reveals the Structure and Evolution of Mating-Type Loci

Pleurotus ostreatus, a widely cultivated edible oyster mushroom, is an ecologically versatile species with applications in biotechnology, agriculture, and food production. It functions as a decomposer and in nutrient-limited conditions it enhances its survival by using a potent toxin to prey on nematodes. Its adaptability is further regulated by sexual reproduction, which follows a tetrapolar mating system governed by two unlinked, multiallelic loci, matA and matB. The two mating-compatible monokaryotic strains PC9 and PC15, derived from the parental dikaryon strain N001, exhibit significant physiological differences. PC9 grows robustly in laboratory conditions, whereas PC15 grows more slowly, making PC9 the preferred strain for research. To advance P. ostreatus as a genetic model, we characterized the mating-type (MAT) loci of both monokaryon strains and developed a congenic strain. We analyzed the MAT loci in multiple P. ostreatus strains, and identified 11 A and 12 B alleles among twelve haplotypes, confirming their multiallelic nature. Using genetic backcrosses, we introgressed the matA and matB loci from PC15 into the PC9 genetic background to generate the congenic strain PC9.15. After sequencing and assembling a high-quality and contiguous genome for PC9.15, we confirmed that the genomes of PC9.15 and PC9 are 99% similar, with the only major difference placed at the matA and matB loci. Author SummaryMushrooms are not just decomposers-they can also be predators. The oyster mushroom Pleurotus ostreatus is an ecologically adaptable species that thrives by breaking down plant material and preying on nematodes using a potent toxin that triggers rapid paralysis of nematode prey. In addition to its ability to switch from saprophyte to predator, another feature contributing to the ecological success of Pleurotus is its reproductive strategy. P. ostreatus reproduces sexually through a tetrapolar mating-type system, governed by two unlinked mating loci, matA and matB. These loci determine mating compatibility and contribute to genetic diversity, yet their precise structure and allelic diversity remain unclear. In this study, we characterized the matA and matB loci in P. ostreatus strains PC9 and PC15 and analyzed MAT loci across multiple strains, confirming their multiallelic nature. To enhance P. ostreatus as a genetic model, we developed the congenic strain PC9.15 by introgressing MAT alleles from PC15 into the PC9 genetic background through genetic backcrosses. Genome sequencing confirmed that PC9.15 closely matches the genome of PC9, except at the MAT loci. This study expands our understanding of mating-type diversity in P. ostreatus, introduces PC9.15 as a valuable tool for genetic studies and controlled crosses, and facilitates the development of P. ostreatus as a model system for fungal biology.

genetics↗

bioRxiv2025

Cuticular collagens mediate cross-kingdom predator-prey interactions between nematodes and trapping fungi

Adhesive interactions, mediated by specific molecular and structural mechanisms, are fundamental to host-pathogen and predator-prey relationships, driving evolutionary dynamics and ecological interactions. Here, we investigate the cellular and molecular basis of adhesion between the nematode Caenorhabditis elegans and its natural predator the nematode-trapping fungus Arthrobotrys oligospora, which employs specialized adhesive nets to capture its prey. Using forward genetic screens, we identified C. elegans mutants that escape fungal traps and revealed the nuclear hormone receptor NHR-66 as a key regulator of fungal-nematode adhesion. Loss-of-function mutations in nhr-66 conferred resistance to fungal trapping through the downregulation of a large subset of cuticular collagen genes. Restoring collagen gene expression in nhr-66 mutants abolished the escape phenotype, highlighting the essential role of these structural proteins in fungal-nematode adhesion. Furthermore, sequence analysis of natural C. elegans populations revealed no obvious loss-of-function variants in nhr-66, suggesting selective pressures exist that balance adhesion-mediated predation risk with physiological robustness. We observed that loss of nhr-66 function resulted in a trade-off of increased hypersensitivity to hypoosmotic stress and cuticular fragility. These findings underscore the pivotal role of structural proteins in shaping ecological interactions and the evolutionary arms race between predator and prey.

evolutionary biology↗

bioRxiv2024

Predation by nematode-trapping fungus triggers mechanosensory-dependent quiescence in C. elegans

Predation can induce behavioral changes in prey, yet the molecular and neuronal mechanisms underlying prey responses remain poorly understood. Here, we investigated how the nematode Caenorhabditis elegans responds to predation by the nematode-trapping fungus, Arthrobotrys oligospora. We found that A. oligospora predation induced quiescence in C. elegans showing rapid cessation of pharyngeal pumping and movement. Calcium imaging revealed that this quiescence was regulated by the activation of sleep-promoting neurons, ALA and RIS. Genetic analyses demonstrated that ALA were essential for pharyngeal pumping inhibition, whereas both ALA and RIS contributed to movement cessation. Transcriptomic analysis in C. elegans showed the upregulation of immune defense genes in response to A. oligospora predation. We demonstrated that mechanosensation was required for pumping inhibition and transcriptomic regulation upon A. oligospora trapping. These findings suggest that physical constraints imposed by fungal traps trigger a stress-induced quiescence and the upregulation of defense genes in C. elegans. We suggest that trapping-induced quiescence might be a predation strategy used by sessile predators to prevail in the evolutionary arms race.

microbiology↗

bioRxiv2020

SNPC-1.3 is a sex-specific transcription factor that drives male piRNA expression in C. elegans

Piwi-interacting RNAs (piRNAs) play essential roles in silencing repetitive elements to promote fertility in metazoans. Studies in worms, flies, and mammals reveal that piRNAs are expressed in a sex-specific manner. However, the mechanisms underlying this sex-specific regulation are unknown. Here we identify SNPC-1.3, a variant of a conserved subunit of the snRNA activating protein complex, as a male-specific piRNA transcription factor in C. elegans. Binding of SNPC-1.3 at male piRNA loci drives spermatogenic piRNA transcription and requires the core piRNA transcription factor SNPC-4. Loss of snpc-1.3 leads to depletion of male piRNAs and defects in male-dependent fertility. Furthermore, TRA-1, a master regulator of sex determination, binds to the snpc-1.3 promoter and represses its expression during oogenesis. Loss of TRA-1 targeting causes ectopic expression of snpc-1.3 and male piRNAs during oogenesis. Thus, sexual dimorphic regulation of snpc-1.3 coordinates male and female piRNA expression during germline development.

developmental biology↗