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Effect of different stress-responsive signaling pathways in the cytokinesis and survival of S. pombe exomer mutants

AutorMoro, Sandra; Hoya, Marta; Sharifmoghadam, M. R.; Pérez, Pilar; Valdivieso, María Henar
Fecha de publicación2015
CitaciónOrganelle Crosstalk in Membrane Dynamics and Cell Signalling (2015)
ResumenThe term exomer refers to a Saccharomyces cerevisiae complex required for the delivery of certain transmembrane proteins to the plasma membrane. Schizosaccharomyces pombe Cfr1p and Bch1p are similar to some exomer components. In the absence of these proteins, S. pombe cells are sensitive to KCl and exhibit a defect in cytokinesis. cfr1Δ and bch1Δ cells are also sensitive to potassium acetate, MgCl2, EGTA, DTT, and tunicamycin. However, the presence of these compounds does not lead to cytokinesis defects. In order to search for genes related to these phenotypes we have performed Synthetic Genetic Arrays. We have found that deleting other genes involved in traffic (apm1+, gga21+, gga22+, get3 +), the channel components cch1+and yam8+, and the GTPase rho3+enhances cfr1Δ and bch1Δ sensitivity to stress. We have also analyzed the effect of eliminating different stress-responsive signaling pathways in the sensitivity of exomer mutants. We have found no relationship between stress sensitivity and calcineurin. On the other hand, eliminating the cell integrity pathway kinase spm1+/pmk1+ and the unfolded protein response kinase ire1+ suppresses sensitivity to potassium acetate and MgCl2. Finally, eliminating the stress response kinase sty1+ enhances sensitivity to KCl and potassium acetate. These results suggest that the sensitivity of the exomer mutants to stress is not mediated by the alteration of a single process, and that their survival to stress requires a complex cellular response.
DescripciónResumen del póster presentado al Biochemical Society Meeting: "Organelle Crosstalk in Membrane Dynamics and Cell Signalling", celebrado en Edimburgo (UK) del 26 al 29 de octubre de 2015.
URIhttp://hdl.handle.net/10261/157330
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