Biology subjects

V, S.

Publications and source records attributed to V, S..

5 recordsLinked to original sources

bioRxiv2025

Reinforcement of speciation by behavioural and reproductive barriers in the Drosophila bipectinata species complex

Speciation mainly depends on different mechanisms involved in reproductive isolation; Understanding such barriers that consistently develop to avoid the fitness cost through reinforcement until the speciation continuum completes helps clarify the role of pre-mating and post-mating isolating mechanisms. The Drosophila bipectinata species complex, comprising four closely related taxa, provides a natural system for studying the interplay of behavioural, sensory, and genetic mechanisms underlying reproductive isolation. In this study, a comprehensive characterization was undertaken on twelve different types of sterile F1 hybrid males among the crosses between four species of Drosophila bipectinata species complex which are experiencing reproductive isolation. Comparing the mating latency and copulation duration among the pure species and hybrids, showed a significant increase in the mating latency of hybrids but the duration of copulation among certain hybrids of Drosophila bipectinata, Drosophila parabipectinata and Drosophila malerkotliana showed no significant reduction in the copulation time and emphasized the strong influence of X chromosome inheritance of hybrid genome. Experimental ablation of antennae demonstrated that male olfactory input is indispensable for heterospecific mating success, consistent with the role of pheromone detection in conspecific recognition, while tarsi ablation revealed striking sex-specific asymmetry: male tarsi removal increased heterospecific success, whereas female tarsi removal abolished mating entirely, highlighting the role of gustatory receptors in female mate choice. Testis dissections further confirmed that post-meiotic defects in hybrids, including failure of spermatid elongation and individualization, these findings demonstrates that reproductive isolation in the D. bipectinata species complex arises from the collective action of multiple barriers, prezygotic isolation mediated by pheromonal and gustatory divergence, and postzygotic sterility driven by spermatogenic failure. Our study underscores how behavioural and physiological divergence interact to reinforce reproductive barriers, providing a comprehensive framework for understanding speciation in Drosophila.

genetics↗

bioRxiv2025

Cis-regulatory divergence and misexpression of spermatogenesis genes underlie hybrid male sterility in the Drosophila bipectinata species complex

Hybrid male sterility (HMS) is one of the most common and earliest forms of postzygotic reproductive isolation in Drosophila, often arising from defects in spermatogenesis linked to regulatory divergence of rapidly evolving male-biased genes. The Drosophila bipectinata species complex (D. bipectinata, D. malerkotliana, D. parabipectinata, and D. pseudoananassae) provides a valuable system to study the speciation paradigm, since, all the twelve F hybrid males are sterile, the precise stage of spermatogenic failure differs among crosses. Here, we integrate cytological, transcriptional, and regulatory sequence analyses to examine the basis of sterility in this sub-complex. Cytological assays revealed that hybrid testes exhibit developmental arrest at different spermatogenesis stages, covering from reduced primary spermatocytes to absence of individualized sperm. Quantitative RT-PCR of seven spermatogenesis genes--aly, bam, sa, dj, topi, can, and Mst98Ca--showed significant downregulation among hybrid males relative to parental species, linking transcriptional misregulation with observed phenotypic defects in spermatogenesis. To test whether regulatory divergence underlies this misexpression, we analyzed [~]1-2 kb promoter regions of five genes (aly, bam, sa, dj, and topi). Motif scans using FIMO identified several lineage-specific turnover of transcription factor binding sites, also PWM-delta analysis revealed substantial interspecific differences in predicted binding strength for many key testis transcription factors. These results demonstrate that HMS in the D. bipectinata complex is consistently associated with spermatogenic arrest and misregulation of genes essential for germline proliferation, meiotic progression, and spermiogenesis. The concordance between expression changes and promoter divergence supports a role for cis-regulatory evolution in hybrid dysfunction, while also leaving open the contribution of trans-acting factors. This study situates the D. bipectinata complex within the broader framework of Drosophila hybrid sterility, extending and highlighting the evolutionary sensitivity of spermatogenesis and regulatory divergence in speciation.

evolutionary biology↗

bioRxiv2024

Diabetes-Tuberculosis Comorbidity Characterized by Reduced Type-II Interferon and Elevated Th17 Responses.

Understanding the perturbed lung immune cells distribution and its functionality in tuberculosis (TB) is well documented; however, limited reports have covered their disruption, if any, in diabetes-tuberculosis (DM-TB) comorbid conditions. Here, we employed single-cell RNA-seq to investigate the molecular mechanisms that govern the heterogeneity in host immune response in DM-TB comorbid conditions. Diabetes is associated with chronic hyperinflammation and reduced lung-infiltrating immune cells, which delays the immune response to Mycobacterial infection. scRNA-seq of lung CD3 and CD11c cells revealed compromised adaptive and innate immunity, with decreased Th1 and M1 macrophage populations in DM-TB mice. A dampened immune response, marked by increased IL-16 signaling and reduced TNF and IFN-II responses, was observed in DM-TB. This study highlights chronic inflammation, hyperglycemia, and dyslipidemia associated with diabetes impairing anti-TB immunity. Selective inhibition of aberrant IL-16 secretion and Th17 cell activation might provide strategies for better managing DM-TB comorbidity.

immunology↗

bioRxiv2023

microRNA-22 displaces ITAFs from the 5'UTR and inhibit the translation of Coxsackievirus B3 RNA

microRNAs play an essential role in gene regulation during virus infections and have major consequences on viral pathogenesis. During RNA virus infections, the host miRNAs can target both host mRNAs and the virus genomic RNA. Using the CVB3 virus as a model, we have investigated how a host miRNA can target viral genomic RNA and act as an antiviral factor limiting the growth of the virus. CVB3 is an RNA virus whose infection causes myocarditis and, eventually, dilated cardiomyopathy. We shortlisted miRNAs with a potential binding site in the CVB3 genomic RNA. Among these, miR-22 was picked for further studies as its binding site was putatively located in a region in the CVB3 5 UTR, important for recruiting ITAFs and ribosomes for IRES-mediated translation. Using mutational analysis and pull-down assays, we first confirmed the binding of miR-22 on the 5UTR. This binding negatively regulated the translation of CVB3 RNA. However, miR-22 binding-defective mutant of CVB3 RNA had no effect of miR-22 overexpression and could translate normally. Moreover, cells from which miR-22 was knocked out, showed a higher level of CVB3 infection as compared to the wild type. We have further demonstrated that the binding of miR-22 interferes with the recruitment of several ITAFs (La, PSF, and PTB) on viral mRNA. This abrogates the spatial structure necessary for ribosome recruitment on the CVB3 RNA, ultimately inhibiting its translation. Also, the level of miR-22 increases 4 hours post-infection, presumably after the synthesis of viral 2A protease, to regulate infection in the host cell more effectively. Along with the direct effect on viral RNA, the altered level of miR-22 affects the level of its cellular targets which might contribute to CVB3 infection. To identify the possible players, we obtained a list of miR-22 targets and performed pathway analysis. Several targets were shortlisted among the top hits and their levels upon CVB3 infection were checked. Protocadherin-1 (PCDH-1), a single-pass transmembrane protein, followed an expected trend, and its levels were significantly downregulated upon CVB3 infection in miR-22 dependent manner. miR-22 mediated suppression of PCDH1 levels during CVB3 infection points towards the possible role of miR-22 in either modulating antiviral signaling or in virus entry, in addition to regulating the viral translation.

molecular biology↗

bioRxiv2019

Biodiversity clock and conservation triangle: Integrative platform for biodiversity monitoring, evaluation, and preemptive conservation intervention

Business-as-usual is no more an option on the table for biodiversity conservation. Disruptive transformation at both policy and polity levels are pressing needs. The possibilities presented by the current wave of information and communication technology can act as travelators to meet the conservation targets. Here, we introduce twin concepts of biodiversity clock and conservation triangle that posit as convergence plane to seamlessly consolidate ongoing discrete efforts and convey real-time biodiversity information in a lucid schematic form. In its present form, the biodiversity clock depicts 12 ecological and 6 biophysical components. The universal consistency in clock-reading facilitates the biodiversity clock to be read and interpreted identically across the world. A ternary plot of the International Union of Conservation of Nature (IUCN) species conservation status is presented as the conservation triangle. Together, the biodiversity clock and the conservation triangle are invaluable in strategizing biodiversity conservation, post-2020. Leveraged smartly, they make possible pre-emptive intervention for biodiversity conservation.

ecology↗