Search bioRxiv⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/405431

Reproductive functions and genetic architecture of the seminal fluid and sperm proteomes of the mosquito Aedes aegypti

Degner, E. C.·Ahmed-Braimah, Y.·Borziak, K.·Wolfner, M. F.·Harrington, L. C.·Dorus, S.
View original source ↗Export metadata ↓

Abstract

The yellow fever mosquito, Aedes aegypti, transmits several viruses, including dengue, Zika, and chikungunya. Some proposed efforts to control this vector involve manipulating reproduction to suppress wild populations or replacing them with disease-resistant mosquitoes. The design of such strategies requires an intimate knowledge of reproductive processes, yet our basic understanding of reproductive genetics in this vector remains largely incomplete. To accelerate future investigations, we have comprehensively catalogued sperm and seminal fluid proteins (SFPs) transferred to females in the ejaculate using tandem mass spectrometry. By excluding female-derived proteins using an isotopic labelling approach, we identified 870 sperm proteins and 280 seminal fluid proteins. Functional composition analysis revealed parallels with known aspects of sperm biology and SFP function in other insects. To corroborate our proteome characterization, we also generated transcriptomes for testes and the male accessory glands--the primary contributors to Ae. aegypti sperm and seminal fluid, respectively. Differential gene expression of accessory glands from virgin and mated males suggests that protein translation is upregulated post-mating. Several SFP transcripts were also modulated after mating, but >90% remained unchanged. Finally, a significant enrichment of SFPs was observed on chromosome 1, which harbors the male sex determining locus in this species. Our study provides a comprehensive proteomic and transcriptomic characterization of ejaculate production and composition and thus provides a foundation for future investigations of Ae. aegypti reproductive biology, from functional analysis of individual proteins to broader examination of reproductive processes.

Source connections

Explore related subjects

genomicsPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Degner, E. C., Ahmed-Braimah, Y., Borziak, K., Wolfner, M. F., Harrington, L. C., Dorus, S.. 2018-08-31. Reproductive functions and genetic architecture of the seminal fluid and sperm proteomes of the mosquito Aedes aegypti. https://doi.org/10.1101/405431

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

KEEP EXPLORING

Related preprints

bioRxiv2026

Recurrent mitotic error and purifying selection shape chromosomal mosaicism across human tissues

Mosaic chromosomal alterations (mCAs) have been extensively studied in cancer and clonal hematopoiesis but less so in healthy solid tissues. Here, we characterized mCAs in 19 tissues across 25 donors (aged 42-89+ years) by analyzing >200x whole-genome sequencing data generated by the Somatic Mosaicism across Human Tissues (SMaHT) Network. Across 722 tissue samples, we identified 1,008 autosomal mCAs >1 Mb in length and ubiquitous losses of sex chromosomes. Surprisingly, the highest levels of Y chromosome loss in males (5-10% cell fraction in elderly donors) were observed in the lung, adrenal gland, and heart. These tissues also tended to experience more X loss in females, revealing a gradient of mitotic error burden across human tissues. Autosomal aneuploidies displayed distinct tissue-specific patterns indicative of negative selection against most events, except in the adrenal gland, in which low-level aneuploidy was pervasive. In contrast to the adrenal gland, testis rarely harbored aneuploidies but frequently experienced low-level copy-neutral loss of heterozygosity (CN-LOH), suggesting increased mitotic recombination in spermatogonial stem cells. Recurrent X chromosome losses within tissues of female donors exhibited allelic skews explained by a combination of genetic and epigenetic effects. Together, these results show that the chromosomal landscape of aging human tissues is shaped by genetics and recurrent mutations, most but not all of which are held in check by purifying selection.

genomics↗
bioRxiv2026

A Chromosome Scale Genome Assembly for the Australian blue mussel Mytilus planulatus

Mussels belonging to the genus Mytilus are among the world's most ecologically and economically important bivalve molluscs. Although the genus most likely originated in the Northern Hemisphere, the evolutionary history of Southern Hemisphere lineages, including the timing and number of colonisation events leading to the extant Australian populations, remains debated. Limited genomic resources have hindered the reconstruction of these evolutionary histories. In Australia, distinguishing native Mytilus planulatus from invasive Mytilus galloprovincialis is critical for biosecurity and conservation, but previous molecular approaches lacked sufficient resolution to resolve species boundaries and hybridisation patterns. Here, we present the first chromosome-scale reference genome for M. planulatus. The assembly consists of 14 chromosomes and over 51,000 annotated protein-coding genes per haplotype. Comparative analysis revealed extensive structural variation and widespread hemizygosity despite a largely conserved chromosomal organisation relative to M. galloprovincialis. Population analyses using SNPs and gene presence-absence variation in resequenced individuals confirmed previously inferred patterns of population structure and establish this reference genome as a valuable resource for future studies of genome evolution, adaptation and population genomics in Mytilus.

genomics↗
bioRxiv2026

An Isogenic iPSC Model of LMNA p.R482W Recapitulates Adipocyte Dysfunction in Familial Partial Lipodystrophy Type 2

Familial partial lipodystrophy type 2 (FPLD2) is a rare autosomal dominant disorder caused by pathogenic variants in LMNA, most commonly p.R482W, and is characterized by selective loss of subcutaneous adipose tissue, severe insulin resistance, and dyslipidemia. The cellular mechanisms underlying adipocyte dysfunction in FPLD2 remain incompletely understood, in part because existing in vitro models rely on patient-derived, non-isogenic cell lines or require non- physiologic transgene overexpression to achieve adipogenic differentiation. Here, we describe a CRISPR/Cas9-edited isogenic iPSC model of FPLD2 in which the heterozygous LMNA c.1444C>T (p.R482W) variant was introduced into a healthy donor-derived iPSC line. Using a transgene-free mesenchymal progenitor differentiation protocol, we generated LMNAp.R482W and isogenic control adipocytes and characterized their transcriptomic and functional phenotypes. Bulk RNA- sequencing demonstrated strong concordance in adipogenesis gene expression between genotypes during differentiation (Pearson {rho} = 0.968), yet LMNAp.R482W adipocytes exhibited significant downregulation of key adipogenic, lipid-handling, and extracellular matrix genes compared to isogenic controls. Functionally, LMNAp.R482W adipocytes showed markedly impaired glucose uptake under both basal and insulin-stimulated conditions, consistent with severe insulin resistance. Seahorse extracellular flux analysis revealed a globally quiescent metabolic state with significantly reduced oxygen consumption rate (126.5 vs. 261.5 pmol/min, p < 0.0001) and extracellular acidification rate (27.6 vs. 46.7 mpH/min, p < 0.0001). To validate these findings in human tissue, gene set enrichment analysis results from the iPSC model were compared to single-nucleus RNA-sequencing data from subcutaneous white adipose tissue biopsies of individuals with FPLD2 carrying the LMNA p.R482W variant. Across 37 mutually significant pathways, 59.5% were concordant between the iPSC model and human adipose tissue, including the pathways most central to FPLD2 pathophysiology: adipogenesis, fatty acid metabolism, oxidative phosphorylation, and inflammatory response. These findings establish this isogenic iPSC system as a faithful cellular model of FPLD2 adipocyte biology and a platform for functional characterization of LMNA variants of uncertain significance.

genomics↗