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Sarmah, H.

Publications and source records attributed to Sarmah, H..

5 recordsLinked to original sources

Salt-induced reduction of hyperswarming motility in Bacillus cereus MHS is associated with reduced flagellation, reduced nanotube formation and reduction in expression of quorum sensing regulator

Bacteria have been known to thrive in challenging environmental niches through diverse phenomena. Swarming is one such favourable adaptation that could help bacteria survive extreme conditions. Therefore, targeting swarming is crucial for improving our understanding of bacterial motility and preventing related infections. Bacillus cereus, which causes food poisoning, has been shown to perform swarming, and salts like NaCl can act as a food preservative to control bacterial growth. In order to explore the possible alterations in the swarming of Bacillus cereus in the presence of salt, the present study encompasses the effect of NaCl on the swarming characteristics of a natural bacterial isolate, Bacillus cereus MHS, with a hyperswarming phenotype. Here we report that the presence of an increased amount of NaCl in growth media could induce a reduction in swarming motility and swarming pattern of MHS on Luria agar plates and the observed reduction in swarming was associated with the reduced flagellation and reduction in bacterial nanotube formation. Gene expression studies supported the phenotypic and ultrastructure observations as the expressions of bfla and ymdb genes, involved in formations of flagella and nanotubes respectively, were found to be reduced in the swarming MHS cells in the presence of increased NaCl in swarm media. It was also observed that the salt-induced reduction in swarming of MHS is associated with the reduced expression of the quorum sensing regulator gene plcR. This study first time reports the bacterial nanotubes in a Bacillus cereus strain and indicates a possible link between the bacterial nanotube formation and hyperswarming phenotype in Bacillus cereus MHS.

microbiology↗

Ephrin Forward Signaling Controls Interspecies Cell Competition in Pluripotent Stem Cells

In the animal kingdom, evolutionarily conserved mechanisms known as cell competition eliminate unfit cells during development. Interestingly, cell competition also leads to apoptosis of donor cells upon direct contact with host cells from a different species during interspecies chimera formation. The mechanisms underlying how host animal cells recognize and transmit cell death signals to adjacent xenogeneic human cells remain incompletely understood. In this study, we developed an interspecies cell contact reporter system to dissect the mechanisms underlying competitive interactions between mouse and human pluripotent stem cells (PSCs). Through single-cell RNA-seq analyses, we discovered that Ephrin A ligands in mouse cells play a crucial role in signaling cell death to adjacent human cells that express EPHA receptors during interspecies PSC co-culture. We also demonstrated that blocking the Ephrin A-EPHA receptor interaction pharmacologically, and inhibiting Ephrin forward signaling genetically in the mouse cells, enhances the survival of human PSCs and promotes chimera formation both in vitro and in vivo. Our findings elucidate key mechanisms of interspecies PSC competition during early embryogenesis and open new avenues for generating humanized tissues or organs in animals, potentially revolutionizing regenerative medicine.

cell biology↗

Foxa2 lineage+ mesendoderm forms a competitive pulmonary mesenchyme niche crucial for generating the entire lungs

Millions suffer from incurable lung diseases, and the donor lung shortage hampers organ transplants. Identifying the crucial lineage and the program for lung organogenesis could facilitate designing whole-lung bioengineering. Using lineage-tracing mice and human iPSC-derived lung-directed differentiation, we revealed that gastrulating Foxa2 lineage contributed to both lung mesenchyme and epithelium formation. Interestingly, Foxa2 lineage-derived cells in the lung mesenchyme progressively increased and occupied more than half of the mesenchyme niche, including endothelial cells, during lung development. Foxa2 promoter-driven, conditional Fgfr2 gene depletion caused the lung agenesis phenotype in mice. Importantly, wild-type donor mouse iPSCs injected into their blastocysts rescued this phenotype by complementing the Fgfr2-defective niche in the lung epithelium and mesenchyme. Donor cell is shown to replace the entire lung epithelial and robust mesenchymal niche during early chimeric lung development, resulting in efficient complementation of the nearly entire lung niche at the late stage of lung development. These results suggest that lung complementation based on the Foxa2 lineage is a unique model for the progressive mobilization of donor cells into both epithelial and mesenchymal lung niches and provides crucial insights for designing new bioengineering strategies to generate whole lungs.

developmental biology↗

A developmental program that regulates mammalian organ size offsets evolutionary distance

Pigs are evolutionarily more distant from humans than mice, but their physiological organs are closest to humans. The molecular program leading to a more than 1,000-fold increase in organ size in pigs and humans over that of mice across evolution has not been elucidated. We generated large-scale transcriptional landscapes throughout swine lung development. Our cross-species single-cell molecular atlas let us discover swine progenitor identities, stage-specific markers, and a core organ-size regulation program (COSRP), well-conserved in swine and humans but less so in mice. Across eight mammalian species, human COSRP promoters showed higher homologies to evolutionary-distant large animals, including pigs, than evolutionary-close small animals. Our study provides a molecular foundation during swine lung development that unveils animal size regulation conserved in the COSRP promoter, independent of genome-wide evolution. COSRP is a critical paradigm for studying thousands-fold changes in biological sizes in evolution, development, cancer, zoology, respirology, organoids, and biotechnology, particularly human-compatible organ generation. One Sentence SummaryA cross-species developmental molecular atlas identified the indicator of lung and animal size beyond evolution

evolutionary biology↗

Loss of CNOT9 begets impairment in gastrulation leading to embryonic lethality

The multi-subunit eukaryotic CCR4-NOT complex imparts gene expression control primarily via messenger RNA (mRNA) decay. Here, we present the role of subunit CNOT9 in target mRNA decay during embryonic development. CNOT9 null mice appear normal by the onset of gastrulation (E7.0), however, exhibit growth and differentiation defects accompanied by extensive cell death by embryonic day 9.5 (E9.5). Sox-2 Cre conditional CNOT9 knockout mice show almost identical phenotype with brief delay in onset and progression, suggesting defects to be epiblast-dominant. Among various identified targets, we show that Lefty2 mRNA expression is post-transcriptionally regulated by CNOT9. Lefty2 3-UTR containing mRNA has significantly higher stability in cells expressing mutant form of CNOT9, relative to cells expressing wild-type CNOT9. In addition, CNOT9 primarily localizes within the cytoplasm and bridges interactions between the CCR4-NOT complex and miRNA-RISC complex in gastrulating embryos.

developmental biology↗