Biology subjects

Sauria, M.

Publications and source records attributed to Sauria, M..

3 recordsLinked to original sources

bioRxiv2026

A Male Expressed Copulatory Plug Increases Female Fertility in Caenorhabditis Nematodes

The genomes of self-fertilizing hermaphrodites offer a unique opportunity to probe why some genes with sex-specific functions are lost while others are maintained. In the androdiecious species, Caenorhabditis elegans, the presence of mate plugging is polymorphic across genetic backgrounds. The production of a mating plug is controlled by a single gene, plg-1, which has male-specific expression. Given that males are present less than 1% of the time, this gene is likely lost through relaxed selection or purifying selection, especially if mate plugging is maintained through intrasexual selection in males as is often hypothesized. We capitalized on a diverse panel of almost 2,000 C. elegans natural strains to show that plg-1 is maintained in at least 61% of genetic backgrounds, despite the androdiecious mating system. Genetic diversity estimates suggest that the loss of plg-1 is correlated with species globalization. We show that hermaphrodite total fecundity is not correlated with plg-1 genotype, indicating that this gene is not being maintained through linkage to a hermaphrodite beneficial gene. We then demonstrate in both C. elegans and the obligate outcrossing species, C. remanei, that the presence of a mating plug does not assure paternity by preventing subsequent males from mating. Instead, females with a mating plug have an extended peak reproductive window and higher fecundity than females without a mating plug. Together, these results indicate that mate plugging is female beneficial. We suggest that this benefit is derived from mating plugs acting as a vulval cover that can inhibit sperm loss during egg laying, thus reducing sperm limitation. Our work indicates that mate plugging may not always invoke male competition and can instead represent reproductive cooperation. More broadly, it demonstrates that male-specific gene expression does not equate to male-specific function, especially in the context of reproductive interactions.

evolutionary biology↗

bioRxiv2018

TADs pair homologous chromosomes to promote interchromosomal gene regulation

Homologous chromosomes colocalize to regulate gene expression in processes including genomic imprinting and X-inactivation, but the mechanisms driving these interactions are poorly understood. In Drosophila, homologous chromosomes pair throughout development, promoting an interchromosomal gene regulatory mechanism called transvection. Despite over a century of study, the molecular features that facilitate chromosome-wide pairing are unknown. The \"button\" model of pairing proposes that specific regions along chromosomes pair with a higher affinity than their surrounding regions, but only a handful of DNA elements that drive homologous pairing between chromosomes have been described. Here, we identify button loci interspersed across the fly genome that have the ability to pair with their homologous sequences. Buttons are characterized by topologically associated domains (TADs), which drive pairing with their endogenous loci from multiple locations in the genome. Fragments of TADs do not pair, suggesting a model in which combinations of elements interspersed along the full length of a TAD are required for pairing. Though DNA-binding insulator proteins are not associated with pairing, buttons are enriched for insulator cofactors, suggesting that these proteins may mediate higher order interactions between homologous TADs. Using a TAD spanning the spinelessd gene as a paradigm, we find that pairing is necessary but not sufficient for transvection. spineless pairing and transvection are cell-type-specific, suggesting that local buttoning and unbuttoning regulates transvection efficiency between cell types. Together, our data support a model in which specialized TADs button homologous chromosomes together to facilitate cell-type-specific interchromosomal gene regulation.

molecular biology↗

bioRxiv2017

Lamins organize the global three-dimensional genome from the nuclear periphery

Lamins are structural components of the nuclear lamina (NL) that regulate genome organization and gene expression, but the mechanism remains unclear. Using Hi-C, we show that lamins maintain proper interactions among the topologically associated chromatin domains (TADs) but not their overall architecture. Combining Hi-C with fluorescence in situ hybridization (FISH) and analyses of lamina-associated domains (LADs), we reveal that lamin loss causes expansion or detachment of specific LADs in mouse ES cells. The detached LADs disrupt 3D interactions of both LADs and interior chromatin. 4C and epigenome analyses further demonstrate that lamins maintain the active and repressive chromatin domains among different TADs. By combining these studies with transcriptome analyses, we found a significant correlation between transcription changes and the changes of active and inactive chromatin domain interactions. These findings provide a foundation to further study how the nuclear periphery impacts genome organization and transcription in development and NL-associated diseases.\n\nHighlightsO_LILamin loss does not affect the overall TAD structure but alters TAD-TAD interactions\nC_LIO_LILamin null ES cells exhibit decondensation or detachment of specific LAD regions\nC_LIO_LIExpansion and detachment of LADs can alter genome-wide 3D chromatin interactions\nC_LIO_LIAltered chromatin domain interactions are correlated with altered transcription\nC_LI

genomics↗