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We measured pseudopod behavior in 5 h starved mutant cells defective in these signaling pathways.

However, we found that mutant cells defective in skelemin binding had unimpaired adhesion and spreading capacity on integrin ligands, suggesting that skelemin binding to integrin was not essential for cell spreading.

Again, U87dn mutant cells defective in both IRE1 kinase and IRE1 RNase activities produced much lower amounts of EREG under basal condition, a partial recovery of EREG transcript accumulation being observed after 4 to 8 h of incubation with tunicamycin.

We found that most of the mutant cells defective in skelemin binding had unimpaired cell adhesion and spreading capacity at the early stages of cell spreading on immobilized fibrinogen.

Therefore, the finding that bck1Δ mutant cells, defective in the MAP kinase of the CWI pathway, could not produce this structure in response to the thermal stress indicates that the morphological process that leads to CS formation is indeed under the control of the CWI pathway.

While mutations that abrogate endocytosis (Δend3, Δrvs167) resulted in significant PI staining in response to heat stress, mutant cells defective for downstream trafficking events such as endosomal sorting and multivesicular body biogenesis (Δvps23), endosomal-vacuolar fusion (Δvam3), and vacuolar degradation (Δpep4) exhibited negligible PI staining in response to heat stress.

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Thus, while rsp5 mutant strains exhibit broad defects in the heat-induced endocytic response, Δart1 mutant cells are defective for the turnover of only a subset of PM proteins.

Rad21 heterozygous mutant cells are defective in homologous recombination (HR -mediated gene targeting and sister cHR -mediatedhangene

Previous work showed that deletion of the yeast ETR1 gene results in mutant cells with defective respiration [32], but that this mutant phenotype is reversible when mutant cells are supplied with active compartmentalized reductases from a number of very different organisms [6], [10], [26], [27].

ubp3 mutant cells are defective in expression of osmoresponsive genes.

Because BRCA1/2 mutant cells are defective in repairing DSBs, PARPi inhibition may result in accumulation of DSBs in these cells and eventually lead to apoptosis.

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