Biology subjects

Dsouza, S.

Publications and source records attributed to Dsouza, S..

8 recordsLinked to original sources

bioRxiv2026

Multi-trophic risk from human superpredators may alter predator-prey coexistence and population dynamics.

Humans are efficient and deadly predators, yet they may also interact with wildlife in non-lethal ways. This study explores how interactions with lethal and non-lethal human "superpredators" alter predator-prey dynamics using an agent-based modelling approach. Our model incorporates both the consumptive (lethal) and non-consumptive (behavioural) effects of humans, as well as of predators on prey. We explored how the replacement of apex predators by humans affects mesopredator-prey dynamics, with particular emphasis on trophic targeting and differences between lethal and non-lethal interactions. We found that human superpredators have a greater effect on model outcomes than apex predators. When superpredators consume mesopredators alone or with prey, the probability of mesopredator-prey coexistence increases to a greater extent than when apex predators consume mesopredators. In contrast, superpredators consuming only prey slightly increases overall extinction risks and reduces coexistence. Non-lethal superpredators, despite eliciting anti-predator responses in mesopredators and prey, had a negligible effect on population dynamics. Our findings demonstrate that human superpredators may functionally replace apex predators when they are lethal. However, non-lethal interactions with humans may not be as ecologically significant as lethal interactions, even when humans induce anti-predator responses.

ecology↗

bioRxiv2026

Chronic TGFβ1 Signaling Drives Aberrant Alveolar-Basaloid Metaplasia through a KRT17-Stratifin migratory complex

Chronic fibrotic disorders like idiopathic pulmonary fibrosis (IPF) are characterized by aberrant alveolar regeneration and severely limited treatment options. Identification of the mechanisms driving aberrant epithelial repair can lead to new viable therapeutic targets. Using integrated single nucleus ATAC- and RNA-sequencing on human lungs and an in vitro model of dysplastic repair, we identify two distinct regenerative trajectories for alveolar type 2 (AT2) cells: a resolvable euplastic repair trajectory and a persistent, non-resolving dysplastic repair trajectory. The latter is governed by a spatially restricted ITGB6/TGF {beta} 1/SMAD3 signaling axis in fibrotic regions of IPF lungs and in murine lungs characterized by chronic epithelial remodeling. Mechanistically, SMAD3 directly regulates dysplastic transitional cell (DTC) markers, including KRT17 and Stratifin. We show that TGF {beta} 1-induced physical interaction between KRT17 and Stratifin at the leading edge of migrating DTCs is essential for their migration. These findings collectively define the molecular regulation of AT2-driven dysplastic regeneration and identify TGF {beta} 1-induced KRT17-Stratifin axis as a central driver of AT2 remodeling and their migration in chronic fibrosis, highlighting a therapeutically targetable signaling axis.

cell biology↗

bioRxiv2025

Out of sight, out of mind: Removal of predators by fisheries alters reef fish behaviour.

Pervasive human activities have led to the extirpation of predator species in many ecosystems. Understanding the extent and mechanisms by which such predator loss influences prey behaviour is critical for predicting the ecological consequences of trophic downgrading. We investigated reef fish behaviour in response to predator presence within and outside a protected area in the South Andaman Islands, India. We used 3D printed models to simulate the presence of two different types of predators; a sit-and-wait predator, a grouper (Mycteroperca rosacea) and a wide-ranging pursuit predator, a barracuda (Sphyraena barracuda). We recorded foraging, vigilance, and movement behaviours of herbivorous and invertivorous fish encountered in each plot. Overall, we found that fish were significantly more vigilant in response to both predator models compared to a non-predator control within protected areas but not outside protected areas. Foraging behaviour was suppressed by the predator treatments; however, herbivorous and invertivorous fish responded differently within protected areas. Fish movement behaviours also differed across predator treatments, prey foraging guilds, and areas. Anti-predator responses are thus highly contingent on habitat and both predator and prey traits. We highlight how the selective removal of predators by humans alters predation risk for prey and hence their risk-sensitive behaviours.

ecology↗

bioRxiv2025

Local extraction of predatory fish may initiate behaviourally mediated trophic cascades in coral reefs in the Andaman Islands.

Humans disproportionately target predators due to their higher economic and social value. This has led to widespread declines of predators in ecosystems worldwide leading to far-reaching effects on ecosystem processes. We investigate how the loss of predators from nearshore ecosystems due to fishing affects individual prey behaviour using a gradient of protection as a natural experiment. We collected data on piscivorous predator assemblages, reef habitats and prey behaviour within and outside two marine protected areas (MPAs) in the South Andaman Islands, India. As expected, predator abundance was significantly greater within MPAs. Similarly, we found greater coral cover and reduced algal cover within MPAs. In response, prey species, which included herbivorous and invertivorous fish, exhibited reduced movement and heightened vigilance inside MPAs. Additionally, prey individuals foraged at higher rates within MPAs. Habitat complexity and resource availability had complex effects on prey behaviours that varied across guilds. Our findings suggest that fishing directly alters the seascape of fear through the removal of predators. Fishing may also shape prey behaviour and ecological interactions indirectly through habitat degradation. Overall, this study highlights the need to study both direct and indirect consequences of human interactions with wild animals to understand their combined impacts on ecosystems.

ecology↗

bioRxiv2025

A Guanine-quadruplex located on the negative strand of the hepatitis C virus facilitates efficient genomic RNA synthesis

Guanine-rich nucleic acids can form a unique secondary structure called Guanine-quadruplexes (G4s). These G4s are conserved across all domains of life and in viruses, where they can play important regulatory roles in the viral lifecycle. In flaviviruses, the (-) strand 3 untranslated region (UTR) is essential for initiating genomic RNA synthesis. Within the (-) strand 3 UTR of hepatitis C virus (HCV), a highly conserved G4 is located within stem-loop IIy (SLIIy), spanning nucleotides 110-131--a region that is essential for efficient replication. Using bioinformatics, we demonstrate that nucleotides 110-131 are highly conserved across HCV genotypes 1-7, and this region within SLIIy can likely adopt a more energetically favorable G4 conformation rather than the predicted hairpin. From biophysical and cell biology experiments, we show that stabilizing the predicted hairpin structure in SLIIy disrupts RNA synthesis, while successive guanine-to-adenine mutations within the G4 sequence impair G4 formation and hinder replication. Combining our findings with prior studies, we propose that the SLIIy G4 plays a crucial role in recruiting NS3 helicase, which is necessary for unwinding RNA structures and facilitating access for NS5B polymerase. The G4 may serve as a regulatory switch that modulates helicase binding and replication efficiency. We propose that in the absence of a stable G4, NS3 recruitment or unwinding is impaired, leading to inefficient RNA unwinding and reduced polymerase activity, ultimately hindering viral replication. These results reveal a previously unrecognized role for G4 structures in the HCV replication cycle, highlighting their importance in regulating (+) strand RNA synthesis. ImportanceHepatitis C virus is a positive-sense single-stranded RNA virus that relies on an intermediate negative strand to generate new genomic RNA. While the last 157 nucleotides of the negative-strand 3 untranslated region are known to be essential for replication, the underlying regulatory mechanisms have remained poorly understood. Our study demonstrates that a highly conserved guanine-rich sequence (107-131 nt) located on the negative strand SLIIy forms a guanine-quadruplex secondary structure that plays a pivotal role in orchestrating viral RNA synthesis. This G4 not only promotes efficient replication but likely acts as a molecular target to recruit the NS3 helicase, thereby allowing access for the NS5B polymerase. Disruption of the G4 structure and stabilization of the stem-loop severely impairs viral replication. These findings reveal an unrecognized layer of post-transcriptional regulation in the HCV lifecycle and establish G4 RNA structures as a critical element in HCV genome replication.

biophysics↗

bioRxiv2024

Are super-predators also super-scary? A systematic review and meta-analysis of animal responses to human interactions

Humans interact with wild animals through lethal and non-lethal activities. While theory predicts that these interactions should alter animal behaviour, the relative magnitude of impact is not well understood. We conducted a systematic review and meta-analysis of the past 30 years of research, focusing on changes in foraging, vigilance, and movement behaviours in wild animals. We found that lethal human activities (e.g., hunting) cause significant behavioural changes, with targeted species increasing vigilance and reducing foraging in affected areas. Active non-lethal activities (e.g., tourism) elicited similar but weaker patterns, with many species showing little to no change in their behavioural responses. In contrast, passive non-lethal interactions (e.g., roads) produced highly variable responses. Overall, human-induced fear elicits responses in wild animals that broadly align with predictions from the risk allocation hypothesis. However, the magnitude and direction of animal responses depend on the type of human activity and the ecological context. The most pronounced behavioural changes occurred where humans posed a direct lethal threat. Gaps in the literature, uneven data within and across species, and limited information on the history or context of interactions currently limit our ability to better predict when and why animals change their behaviour in response to humans.

animal behavior and cognition↗

bioRxiv2022

A cross taxonomic comparison of bird and butterfly communities of Tamhini Wildlife Sanctuary across two decades.

Human disturbance can alter the structure and function of ecological communities. We studied bird and butterfly communities of Tamhini wildlife sanctuary to understand the effects two decades of changing land use and management. We replicated a previous study conducted between 1998 and 2001, sampling 7 line transects every fortnight between April 2016 and April 2017. We analyzed the diversity and structure of functional groups and compared our findings to previous surveys. Species diversity increased for both taxa, however, community composition was significantly different across studies. Changing land may affect multiple trophic levels and alter community assembly and ecosystem function.

ecology↗

bioRxiv2020

Inhibition of ITK differentiates GVT and GVHD in allo-HSCT

Allogeneic hematopoietic stem cell transplantation is a life-saving treatment for many malignant and nonmalignant diseases. Donor T cells contained within the graft prevent tumor recurrence via graft-versus-tumor (GVT) effects, however, also cause graft-versus-host disease (GVHD). Novel treatment strategies are therefore needed to allow maintenance of GVT while suppressing GVHD. Here we show using murine models, that targeting IL-2-inducible T cell kinase (ITK) in donor T cells reduces GVHD while preserving the beneficial GVT effects. Donor T cells from Itk-/- mice exhibit significantly reduced production of inflammatory cytokines and migration to GVHD target organs such as liver and small intestine, while maintaining GVT efficacy against primary B-ALL tumors. Itk-/- T cells exhibited reduced expression of IRF4 and decreased JAK/STAT signaling activity, but preserved cytotoxicity, which was accompanied by upregulation of Eomesodermin (Eomes), which was necessary for GVT function. A novel peptide inhibitor ITK signaling is also able to prevent GVHD. This novel peptide inhibitor also reduced cytokine production in mice and human T cells. Altogether, our data suggest that inhibiting ITK could be a therapeutic strategy to reduce GVHD while preserving the beneficial GVT effects following allo-HSCT treatment. Key PointsO_LIInhibiting ITK by a novel peptide significantly reduces GVHD but retains GVT. C_LIO_LIITK deficient donor T cells exhibit minimal GVHD, but maintain GVT activity. C_LIO_LIITK deficient donor T cells exhibit significantly reduced production of inflammatory cytokines and migration to GVHD target organs. C_LIO_LIEomes is required for GVT effect. C_LI

immunology↗