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Biology subjects

Jahnavi, S.

Publications and source records attributed to Jahnavi, S..

2 recordsLinked to original sources

Diverse ancestral myosin motors generate and segregate distinct types of nanocluster-rich domains at the plasma membrane

Molecular organization of the plasma membrane (PM) at nano and micron scales is critical for its function in all living cells. This emerges not only from the self-assembly of lipids and proteins but also from active forces originating in the underlying cytoskeletal cortex. These forces drive membrane molecules into non-equilibrium steady state patterns such as nanoclusters. However, the molecular agents connecting membrane organization with cytoskeletal dynamics and stresses have remained unknown. Here we show that two classes of ubiquitous ancestral non-muscle myosins are deployed for the organization of different types of membrane components. Inner-leaflet localized Class I myosins link outer-leaflet GPI-anchored molecules to juxta-membrane actin-filaments, whereas the more cortically-localized Class II myosins operate on transmembrane proteins endowed with actin-binding capacity. Consistent with an active Flory Huggins theory for phase separation, these observations show that the distinct motor-driven membrane molecules generate spatially segregated mesoscale domains, enriched in nanoclusters derived from different myosin classes. Moreover, chemically reversible post-translational modifications such as palmitoylation enable concatenation of these domains by enhancing affinity of the membrane domain constituents for each other. We anticipate that the segregation potential of the ATP-fueled cell membrane is made available for the crucial purpose of modulating information transduction because it can be regulated in space and time during the construction of signaling cascades, underpinning functional plasma membrane organization.

cell biology↗

Niclosamide inhibits SARS-CoV2 entry by blocking internalization through pH-dependent CLIC/GEEC endocytic pathway

Many viruses utilize the host endo-lysosomal network to infect cells. Tracing the endocytic itinerary of SARS-CoV2 can provide insights into viral trafficking and aid in designing new therapeutic targets. Here, we demonstrate that the receptor binding domain (RBD) of SARS-CoV2 is internalized via the clathrin and dynamin-independent, pH-dependent CLIC/GEEC (CG) endocytic pathway. Endosomal acidification inhibitors like BafilomycinA1 and NH4Cl, which inhibit the CG pathway, strongly block the uptake of RBD. Using transduction assays with SARS-CoV2 Spike-pseudovirus, we confirmed that these acidification inhibitors also impede viral infection. By contrast, Chloroquine neither affects RBD uptake nor extensively alters the endosomal pH, yet attenuates Spike-pseudovirus entry, indicating a pH-independent mechanism of intervention. We screened a subset of FDA-approved acidification inhibitors and found Niclosamide to be a potential SARS-CoV2 entry inhibitor. Niclosamide, thus, could provide broader applicability in subverting infection of similar category viruses entering host cells via this pH-dependent endocytic pathway.

cell biology↗