Biology subjects

Tanwar, A.

Publications and source records attributed to Tanwar, A..

2 recordsLinked to original sources

bioRxiv2022

Toroidal displacement of Klebsiella pneumoniae by Pseudomonas aeruginosa is a unique mechanism to avoid competition for iron

Competition for resources is one of the major drivers for evolution and retention of new traits in microbial communities. Quorum-dependent traits of opportunistic human pathogen Pseudomonas aeruginosa allow it to survive and thrive in nature. Here, we report a unique surfactant-driven pushing mechanism that P. aeruginosa employs specifically against Klebsiella pneumoniae. The pushing is accomplished in a manner that is dependent on nutrient limitation and quorum sensing. We find that P. aeruginosa employs neither proteases nor toxic secondary metabolites against K. pneumoniae. Rhamnolipid biosurfactant appears to be the only factor required to displace Klebsiella effectively. Both rhamnolipid production and the pushing ability of P. aeruginosa are suppressed by iron supplementation. We show that both these bacteria produce several siderophores in minimal medium and rapidly deplete iron. Under these conditions, P. aeruginosa pushes Klebsiella away from the substratum using rhamnolipid, reducing the competition for iron. Our study describes a unique quorum and iron-responsive mechanism in P. aeruginosa to support its own growth during resource competition.

microbiology↗

bioRxiv2022

Synergistic Regulation of Notch Signaling by Different O-Glycans Promotes Hematopoiesis

Glycosylation of Notch receptors by O-fucose glycans regulates Notch ligand binding and Notch signaling during hematopoiesis. However, roles in hematopoiesis for other O-glycans that modify Notch receptors have not been determined. Here we show that the EGF domain-specific GlcNAc transferase EOGT is required in mice for the optimal production of lymphoid and myeloid cells. The phenotype of Eogt null mice was largely cell-autonomous, and Notch target gene expression was reduced in T cell progenitors. Moreover, EOGT supported residual Notch signaling following conditional deletion of Pofut1 in hematopoietic stem cells (HSC). Eogt:Pofut1 double mutant HSC had more severe defects in bone marrow, and in T and B cell development in thymus and spleen, compared to deletion of Pofut1 alone. The combined results show that EOGT and O-GlcNAc glycans are required for optimal hematopoiesis and T and B cell development, and that they act synergistically with POFUT1 and O-fucose glycans to promote Notch signaling in lymphoid and myeloid differentiation. Key pointsO_LIO-GlcNAc glycans and EOGT promote lymphopoiesis and myelopoiesis C_LIO_LIEOGT supports Notch signaling in the absence of POFUT1 and O-fucose glycans C_LI

immunology↗