Biology subjects

Saha, M. K.

Publications and source records attributed to Saha, M. K..

4 recordsLinked to original sources

bioRxiv2025

Impact of Soil Salinity on Microbial Community Composition in Coastal Agricultural lands of Bangladesh: A Metagenomic Approach

A significant obstacle to agricultural productivity is soil salinity, especially in coastal areas where the problem is made worse by climate change and rising sea levels. This study investigates the impact of salinity on microbial community structure and function in agricultural soils from Kuakata, Bangladesh, using 16S rRNA metagenomic sequencing technique. Both saline (EC > 4 dS/m) and non-saline (EC < 1.5 dS/m) areas had soil samples taken; saline soils showed symptoms of crop stress, such as yellowing and blackish discoloration. In comparison to their non-saline counterparts, our investigation showed that saline soils had much reduced microbial diversity and different community compositions. Both soil types were dominated by Proteobacteria and Chloroflexi, while saline soils displayed an enrichment of anaerobic texa (e.g., Desulfobacterota, Pseudomonas) and sulfate-reducing bacteria (e.g., Desulfobacterota, Deferrisomatota). Interestingly, saline soils had a much larger percentage of anaerobic microorganisms (36.4%) than non-saline soils (29.3%) which might results in enhanced denitrification, sulphate reduction, and hydrogen sulphide buildup. These processes disrupt nutrient cycling, lower organic matter decomposition and create toxic conditions for plant growth, ultimately contributing to crop failure. This study provides an insight into the distinct microbial composition in saline and non-saline samples, which can assist in understanding the role of microbial populations in agriculture in saline environments.

microbiology↗

bioRxiv2024

Heat-killed probiotic Levilactobacillus brevis MKAK9 and its exopolysaccharide promote longevity by modulating aging hallmarks and enhancing immune responses in Caenorhabditis elegans

BackgroundProteostasis is a critical aging hallmark responsible for removing damaged or misfolded proteins and their aggregates by improving proteasomal degradation through the autophagy-lysosome pathway (ALP) and the ubiquitin-proteasome system (UPS). Research on the impact of heat-killed probiotic bacteria and their structural components on aging hallmarks and innate immune responses is scarce, yet enhancing these effects could potentially delay age- related diseases. ResultsThis study introduces a novel heat-killed Levilactobacillus brevis strain MKAK9 (HK MKAK9), along with its exopolysaccharide (EPS), demonstrating their ability to extend longevity by improving proteostasis and immune responses in wild-type Caenorhabditis elegans. We elucidate the underlying mechanisms through a comprehensive approach involving mRNA- and small RNA sequencing, proteomic analysis, lifespan assays on loss-of- function mutants, and quantitative RT-PCR. Mechanistically, HK MKAK9 and its EPS resulted in downregulation of the insulin-like signaling pathway in a DAF-16-dependent manner, enhancing protein ubiquitination and subsequent proteasomal degradation through activation of the ALP pathway, which is partially mediated by microRNA mir-243. Importantly, autophagosomes engulf ubiquitinylated proteins, as evidenced by increased expression of the autophagy receptor sqst-3, and subsequently fuse with lysosomes, facilitated by increased levels of the lysosome-associated membrane protein (LAMP) lmp-1, suggesting the formation of autolysosomes for degradation of the selected cargo. Moreover, HK MKAK9 and its EPS activated the p38 MAPK pathway and its downstream SKN-1 transcription factor, which are known to regulate genes involved in innate immune response (thn-1, ilys-1, cnc-2, spp-9, spp-21, clec-47, and clec-266) and antioxidation (sod-3 and gst-44), thereby reducing the accumulation of reactive oxygen species (ROS) at both cellular and mitochondrial levels. Notably, SOD-3 emerged as a transcriptional target of both DAF-16 and SKN-1 transcription factors. ConclusionOur research sets a benchmark for future investigations by demonstrating that heat-killed probiotic and its specific cellular component, EPS, can downregulate the insulin- signaling pathway, potentially improving the autophagy-lysosome pathway (ALP) for degrading ubiquitinylated proteins and promoting organismal longevity. Additionally, we discovered that increased expression of microRNA mir-243 regulates insulin-like signaling and its downstream ALP pathway. Our findings also indicate that postbiotic treatment may bolster antioxidative and innate immune responses, offering a promising avenue for interventions in aging-related diseases.

microbiology↗

bioRxiv2023

Small Molecule Inhibitors Targeting Methyltransferase-Like (METTL) Proteins Against Hepatocellular Carcinoma: A Comprehensive DrugRepurposing Approach

An efficient and durable multi-targeted therapeutic drug against hepatocellular carcinoma (HCC) has recently been a growing concern for tackling the chemoresistance of approved anti-HCC drugs. Recent studies indicated that methyltransferase-like (METTL) proteins including METTL1, METTL3, METTL6, METTL16, and METTL18, have overexpressed and associated with the progression of HCC malignancy, and making them excellent biomarkers. Here, we present a series of bioinformatics study including novel compound repurposing approach, molecular docking, pharmacophore modeling, and molecular dynamic simulation, which revealed two first-in-class highly potent catalytic multi-target inhibitors (ZINC70666503 and ZINC13000658 with 87% and 82% drug scores, respectively) of methyltransferase-like proteins. Comparatively, these two inhibitors showed a notable binding affinity against studied METTL proteins. Furthermore, ADME and toxicity analysis suggested that these two commercially available compounds have good drug-likeliness properties with no potent toxic effects. Of note, the molecular dynamics study supported their conformational stability and high selectivity at the pocket of proteins adenosine moiety of S-Adenosyl Methionine. However, this comprehensive analysis needs in vivo validation to facilitate multi-targeting therapeutic development against hepatocellular carcinoma.

cancer biology↗

bioRxiv2021

A vitamin D-RelB/NF-κB pathway limits Chandipura virus multiplication by rewiring the homeostatic state of autoregulatory type 1 interferon-IRF7 signaling

Besides its functions in the skeletomuscular system, vitamin D also promotes protective immunity against viral pathogens. Viral sensing by mammalian cells triggers nuclear activation of RelA/NF-{kappa}B and IRF3 factors, which collaborate in mediating the early induction of antiviral type 1 interferons (T1-IFNs). Autocrine T1-IFN signaling further accumulates otherwise negligibly expressed IRF7 in virus-infected cells that then sustains T1-IFN production in a positive feedback. Surprisingly, prior cell-culture studies revealed that vitamin D actually suppresses signal-induced RelA activation. Indeed, it remains unclear how vitamin D limits viral multiplication in a cell-autonomous manner. Here, we examined the role of vitamin D in controlling cellular infections by the Chandipura virus (CHPV), a cytoplasmic RNA virus implicated in human epidemics. We found that vitamin D conditioning produced an altered cell state less permissive for CHPV multiplication because of the heightened expression of T1-IFNs. It is thought that viruses also induce a distinct RelB/NF-{kappa}B activity, which counteracts RelA-driven T1-IFN expressions in infected cells. Our analyses instead characterized a basal nuclear RelB activity, which was downregulated upon vitamin D-mediated suppression of RelB synthesis. Interestingly, this vitamin D-RelB pathway provoked IRF7-mediated positive autoregulation augmenting constitutive T1-IFN expressions even in the absence of viral infections. Accordingly, RelB deficiency rendered redundant, while IRF7 depletion abrogated antiviral vitamin D actions. In sum, our study suggests that the homeostatic state of the signaling circuitry comprising of the NF-{kappa}B and T1-IFN pathways connects micronutrients to antiviral immunity at the cellular level. Significance statementVitamin D limits viral infections, but the underlying mechanism remains unclear. Linking micronutrients to antiviral immunity, Ratra et al. characterize an immune signaling circuitry engaged by vitamin D that generates a cellular state less permissive to infections by Chandipura virus, a pathogen of public health importance.

immunology↗