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Abella Guerra, M.

Publications and source records attributed to Abella Guerra, M..

2 recordsLinked to original sources

The P4-ATPase Drs2 regulates the homeostasis of Atg9

Multisubunit Tethering Complexes (MTCs) are a set of conserved protein complexes that tether transported vesicles at the acceptor membrane. Interactions with other components of the trafficking machinery regulate MTCs through mechanisms that are just partially understood. Here we systematically investigate the interactome that regulates the function of MTCs. We found that P4-ATPases, a family of lipid transporters involved in the biogenesis of vesicles, interact with MTCs that participate in the anterograde and retrograde transport at the Golgi, such as TRAPPIII. We used the lipid flippase Drs2 as a model to investigate the mechanism and biological relevance of such interplay during the transport of Atg9 vesicles. Binding to the N-terminal tail of Drs2 stabilizes TRAPPIII on membrane compartments loaded with Atg9 and it is required for the delivery of Atg9 during selective autophagy, a role that is independent of previously reported functions of the P4-ATPase. This mechanism relies on the I(S/R)TTK motif nested in the N-terminal tail cavity of Drs2, a motif that is required for the interaction with MTCs.

cell biology

Force requirements of endocytic vesicle formation

Mechanical forces are integral to many cellular processes, including clathrin-mediated endocytosis, a principal membrane trafficking route into the cell. During endocytosis, forces provided by endocytic proteins and the polymerizing actin cytoskeleton reshape the plasma membrane into a vesicle. Assessing force requirements of endocytic membrane remodelling is essential for understanding endocytosis. Here, we determined forces applied during endocytosis using FRET-based tension sensors integrated into the major force-transmitting protein Sla2 in yeast. We measured force of approx. 10 pN transmitted over Sla2 molecule, hence a total force of 450-1300 pN required for endocytic vesicle formation. Importantly, decreasing cell turgor pressure and plasma membrane tension reduced force requirements of endocytosis. The measurements in hypotonic conditions and mutants lacking BAR-domain membrane scaffolds then showed the limits of the endocytic force-transmitting machinery. Our study provides force values and force profiles critical for understanding the mechanics of endocytosis and potentially other key cellular membrane-remodelling processes.

cell biology