%0 Journal Article %T Functional and genetic interactions of TOR in the budding yeast Saccharomyces cerevisiae with myosin type II-deficiency (myo1¦¤) %A Glorivee Pag¨¢n-Mercado %A Ednalise Santiago-Cartagena %A Pearl Akamine %A Jos¨¦ R Rodr¨ªguez-Medina %J BMC Cell Biology %D 2012 %I BioMed Central %R 10.1186/1471-2121-13-13 %X Here we proved that TORC1 signaling was down regulated in the myo1¦¤ strain. While a tor1¦¤ mutant strain had increased viability relative to myo1¦¤, a combined myo1¦¤tor1¦¤ mutant strain showed significantly reduced cell viability. Synthetic rescue of the tor2-21ts lethal phenotype was observed in the myo1¦¤ strain in contrast to the chs2¦¤ strain, a chitin synthase II null mutant that also activates the PKC1 CWIP and exhibits cytokinesis defects very similar to myo1¦¤, where the rescue effect was not observed. We observed two pools of Slt2p, the final Mitogen Activated Protein Kinase (MAPK) of the PKC1 CWIP; one pool that is up regulated by heat shock and one that is up regulated by the myo1¦¤ stress. The cell wall stress sensor WSC1 that activates PKC1 CWIP under other stress conditions was shown to act as a negative regulator of TORC1 in the myo1¦¤ mutant. Finally, the repression of TORC1 was inversely correlated with the activation of PKC1 in the myo1¦¤ strain.Regulated expression of TOR1 was important in the activation of the PKC1 CWIP in a myo1¦¤ strain and hence its survival. We found evidence that the PKC1 and TORC1 pathways share a common upstream regulator associated with the cell wall stress sensor WSC1. Surprisingly, essential TORC2 functions were not required in the myo1¦¤ strain. By understanding how yeast mounts a concerted stress response, one can further design pharmacological cocktails to undermine their ability to adapt and to survive. %K PKC1 %K SLT2/MPK1 %K WSC1 %K Tor2-21 %K Fungal cell wall %U http://www.biomedcentral.com/1471-2121/13/13/abstract