bioRxiv Science⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2024.11.14.623542

TSSK homologue regulates the expression of protamine and mosquito testes specific genes in Anopheles stephensi

Meghwanshi, K. K.·Choudhary, C.·Rohilla, P.·Dixit, R.·Saxena, V.·Shukla, J. N.
View original source ↗Export metadata ↓

Abstract

The testis-specific serine/threonine-protein kinase (tssk) gene is known to play an important role in spermiogenesis in mammals. This study identifies tssk homologues, As_tssk3 and Aea_tssk1 in Anopheles stephensi and Aedes aegypti, respectively. Both As_tssk3 and Aea_tssk1 were found to express in a male-specific manner throughout the development. Efficient knockdown in the expression of As_tssk3 gene was observed upon feeding An. stephensi larvae with target dsRNA. As_tssk3 knockdown led to a reduced sperm reservoir in male adults. Additionally, the knockdown of As_tssk3 resulted in the reduced expression of two male specifically expressed genes, protamine & mosquito testes specific (mts- a sperm-specific marker) homologues of An. stephensi. In-silico interaction analysis suggests that As_TSSK3 protein interacts with the Nucleosome Assembly Protein1 like-4 (NAP1like-4), a putative transcription factor. We hypothesize that As_TSSK3 regulates the transcription of protamine and mts genes via NAP, as both NAP and protamine have previously been shown to function in the establishment and maintenance of chromatin dynamics, in independent studies. The study presented here is the first report of characterisation of tssk homologues in any mosquito species. The knockout studies and phosphorylation assays would provide more insights to explore the mechanism by which As_tssk3 regulates protamine and mts genes in Anopheles stephensi. HighlightsO_LIThis study identifies the tssk homologues in Ae. aegypti and An. stephensi and showed their male-specific expression in both the mosquito species. C_LIO_LIdsRNA mediated knockdown of As_TSSK3 resulted into the males with a reduced size of sperm reservoir. C_LIO_LIdsRNA mediated knockdown of As_TSSK3 led to the reduction in the expression of As_prot and As_mts, homologues of protamine and mosquito testis specific, genes in An. stephensi. C_LIO_LIIn-silico studies suggest that As_TSSK3 regulates the expression of As_prot and As_mts genes via NAP. C_LI

Source connections

Explore related subjects

geneticsPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Meghwanshi, K. K., Choudhary, C., Rohilla, P., Dixit, R., Saxena, V., Shukla, J. N.. 2024-11-15. TSSK homologue regulates the expression of protamine and mosquito testes specific genes in Anopheles stephensi. https://doi.org/10.1101/2024.11.14.623542

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

Large language model-based bibliometric evaluation of population descriptors in human genetics

As the use of population descriptors such as race, ethnicity, and ancestry have become increasingly common in modern genetics research, there have been growing calls to critically examine their use. Most notably, in 2023, the National Academies of Science, Engineering, and Medicine (NASEM) published a report titled Using Population Descriptors in Genetics and Genomics Research: A New Framework for an Evolving Field, which included eight specific and actionable recommendations for researchers to implement the ethical and accurate use of population descriptors in genetic research. Here, we use the 2023 NASEM report as a benchmark to analyze the use of population descriptors in genome-wide association studies (GWAS). We develop a general toolkit for large language model-based bibliometrics, operationalize the report's recommendations into an evaluation framework, and apply this framework to evaluate all 4,007 papers from the GWAS Catalog published between 2007 and 2025 with full text available on PubMedCentral. We find significant improvements in adherence to NASEM report recommendations over time. However, most improvements predate the publication of the NASEM report itself, suggesting the report functioned primarily as a synthesis of existing best practices rather than a catalyst for change. We conclude by highlighting opportunities for growth in the field of human genetics.

genetics↗
bioRxiv2026

Mitigating biases of rescaling in forward-in-time population genetic simulations

Forward-in-time population genetic simulations are widely used in evolutionary analyses, but simulating large populations and long genomic regions remains computationally demanding. To reduce this cost, parameter rescaling is widely employed, in which the original evolutionary process is approximated by one with a smaller population size and fewer generations. Recently, several studies using the SLiM simulator have raised concerns about the accuracy of this rescaling approach. In this study, we show that many of the biases reported in these studies can be mitigated by using a different simulation algorithm. These results reveal that the accuracy of parameter rescaling depends on how well the simulation algorithm preserves diffusion-limit properties under rescaling.

genetics↗
bioRxiv2026

OPA1 controls mitochondrial dysfunction-driven liver fibrosis in MASLD

Progressive hepatic fibrosis is the principal determinant of morbidity and mortality in metabolic dysfunction-associated steatotic liver disease and steatohepatitis (MASLD/MASH). Mitochondrial dysfunction is a hallmark of MASH, and the release of mitochondrial damage-associated molecular patterns (mito-DAMPs) from injured hepatocytes can promote fibrosis. However, how mitochondrial dynamics and quality control shape the fibrotic response in MASLD/MASH remains unclear. Here, through large-scale genomic analyses of mitochondrial genes governing mitophagy, fusion and fission in human MASLD, with a power-equivalent sample size of approximately 700,000 individuals, we identify a strong association between hepatic fibrosis and the mitochondrial fusion factor dynamin-like GTPase optic atrophy 1 (OPA1). OPA1 transcripts and protein abundance in the liver epithelium were progressively dysregulated with advancing fibrosis. In mice, hepatocyte-specific OPA1 loss alone was sufficient to induce hepatic stellate cell activation and fibrosis in zone 3, promoted the release of mito-DAMPs into the circulation and exacerbated fibrosis in experimental MASH. These findings identify OPA1 as a central regulator of the hepatic fibrotic response and connect defective mitochondrial homeostasis to mito-DAMP release, hepatic stellate cell activation and fibrosis in MASLD.

genetics↗