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Biology subjects

Suri, V.

Publications and source records attributed to Suri, V..

3 recordsLinked to original sources

Unbounding fish: Assessing vulnerability to overexploitation for transboundary fish populations

SummeryGlobally coastal fisheries are managed according to political jurisdictions of nations and their provinces. This practice often results in multiple states/provinces managing a single genetically distinct fish population autonomously and without coordination. In multi-species, decentralized and data poor fisheries such management lead to poor assessment and eventually overharvest of fish. To assess overexploitation risk for such interjurisdictional populations, we propose a risk indicator IRIIS which incorporates 1) species-specific vulnerability 2) distribution of genetically-distinct populations with respect to jurisdictional boundaries and 3) differences in management practices across jurisdictions. As a case study we evaluated overexploitation risk for individual populations of nine commonly caught fish species spanning across multiple jurisdictions along Indias west coast. Our results indicate that interjurisdictional differences in management alters innate biological susceptibility. IRIIS is also sensitive to population-level differences and policy changes. Our analyses emphasize the need for population-level assessments and interjurisdictional cooperation to achieve sustainable fisheries. Science and society statementCoastal fisheries worldwide are managed through politically defined maritime jurisdictions, while fish populations are structured by biological processes such as dispersal, ocean currents, and natural barriers. This fundamental mismatch between biological population boundaries and jurisdictional management boundaries often results in the same population being exploited under multiple, uncoordinated governance regimes. In the context of the global overfishing crisis, such governance fragmentation can lead to inaccurate stock assessments and heightened risk of local population collapse. This challenge is particularly acute in developing and tropical countries, where fisheries are multispecies, data-limited, and increasingly decentralized to support community-based governance. While decentralization promotes social justice, it can inadvertently intensify the misalignment between biological and administrative boundaries, complicating sustainable management. In this manuscript, we introduce a robust framework -- the Integrative Risk Indicator for Interjurisdictional Stocks (IRIIS) -- which has a high applicability for multispecies, data-poor, and decentralized fisheries. Building on, and extending beyond, species-level Productivity Susceptibility Analysis (PSA), IRIIS integrates population genomics to delineate biologically meaningful population boundaries and combines these with fisheries policies and regulations across jurisdictions to quantify management-associated risks of overexploitation at the population level. We apply IRIIS to case studies of nine commercially important fish species harvested along the west coast of India. Our results demonstrate that the framework can (i) distinguish differential vulnerability among populations of the same species, (ii) explicitly capture management disparities across jurisdictions exploiting shared populations, and (iii) detect sensitivity to temporal changes in fisheries policies. By linking genomics, governance, and risk assessment, IRIIS provides a practical framework for identifying interjurisdictional management gaps and actionable entry points for policy coordination. This approach is particularly relevant for the Global South, where reconciling social equity objectives with ecological sustainability is both essential and challenging.

ecology↗

The atypical cadherin FAT1 is a novel regulator of STAT1, driving its pro-tumorigenic effect via the STAT1/PDCD4 axis in glioblastoma

FAT1 is an atypical cadherin that has been shown to act both as an oncogene and a tumour suppressor gene (TSG) in different tumor types. We have earlier shown that upregulated FAT1 acts as an oncogene in glial tumors by promoting pro-tumorigenic inflammation and EMT in primary human glioblastoma and in cell lines. One effect was through the suppression of the Tumor Suppressor Gene (TSG), Programmed Cell Death 4 (PDCD4). Here, we have studied how, in glioblastoma, upregulated FAT1 affects downstream events that control PDCD4 expression. In silico analysis of the PDCD4 promoter revealed multiple STAT1 binding sites. We also found a positive correlation in mRNA levels of STAT1 and FAT1 in the Glioblastoma databases, as well as in resected patient derived tumor samples by qPCR. Increased FAT1 as well as STAT1 were associated with poor prognosis in these data bases. In the glioblastoma cell lines LN229 and U87MG, FAT1 knockdown resulted in decreased STAT1 expression. Also, STAT1 knockdown resulted in increased PDCD4 expression, implying that STAT1 may mediate FAT1s role in suppressing PDCD4. Further, ChIP experiments showed that STAT1 protein binds to the PDCD4 promoter and upon FAT1 knockdown, STAT1 binding to the PDCD4 promoter reduces. As for FAT1, STAT1 knockdown also reduces the expression of pro-inflammatory cytokines and EMT markers, also migration and invasion of glioma derived cell lines. This work identifies STAT1 as a novel downstream mediator of FAT1 which mediates its pro-tumorigenic action in suppressing the TSG, PDCD4.

cancer biology↗

Limited Environmental Serine Confers Sensitivity to PHGDH Inhibition in Brain Metastasis

A hallmark of metastasis is the adaptation of tumor cells to new environments. Although it is well established that the metabolic milieu of the brain is severely deprived of nutrients, particularly the amino acids serine and its catabolite glycine, how brain metastases rewire their metabolism to survive in the nutrient-limited environment of the brain is poorly understood. Here we demonstrate that cell-intrinsic de novo serine synthesis is a major determinant of brain metastasis. Whole proteome comparison of triple-negative breast cancer (TNBC) cells that differ in their capacity to colonize the brain reveals that 3-phosphoglycerate dehydrogenase (PHGDH), which catalyzes the rate-limiting step of glucose-derived serine synthesis, is the most significantly upregulated protein in cells that efficiently metastasize to the brain. Genetic silencing or pharmacological inhibition of PHGDH attenuated brain metastasis and improved overall survival in mice, whereas expression of catalytically active PHGDH in a non-brain trophic cell line promoted brain metastasis. Collectively, these findings indicate that nutrient availability determines serine synthesis pathway dependence in brain metastasis, and suggest that PHGDH inhibitors may be useful in the treatment of patients with cancers that have spread to the brain. Statement of SignificanceOur study highlights how limited serine and glycine availability within the brain microenvironment potentiates tumor cell sensitivity to serine synthesis inhibition. This finding underscores the importance of studying cancer metabolism in physiologically-relevant contexts, and provides a rationale for using PHGDH inhibitors to treat brain metastasis.

cancer biology↗