Research Article

The Cell Wall Sensors Mtl1, Wsc1, and Mid2 Are Required for Stress-Induced Nuclear to Cytoplasmic Translocation of Cyclin C and Programmed Cell Death in Yeast

Figure 7

Mtl1 overexpression suppresses mid2Δ wsc1Δ signaling defect. (a) Phosphorylation (top panels) and immunoprecipitation (bottom panels) of Slt2-HA in wild-type strain (RSY10) following 0.4 mM and 0.8 mM H2O2 treatment as indicated. (b) A mid2Δ wsc1Δ mutant (RSY1844) harboring an integrated copy of MTL1 under the control of the GAL1 promoter and cyclin C-myc (pLR337) was grown to midlog in raffinose. The culture was split and treated with either 2% galactose or glucose for 2 h before the addition of 0.4 mM H2O2. Cyclin C levels were monitored by Western blot analysis of immunoprecipitates. Tub1 levels were used as a loading control. (c) Model of combinatorial signal transduction pathway control for cyclin C regulation. Sensors associated with the plasma membrane (PM) and cell wall (CW) are indicated. Sensor activity in response to low, high, and extreme ROS exposure is indicated. Under low stress conditions, the combined signals from both Mtl1 and Mid2/Wsc1 are required to trigger cyclin C relocalization and destruction. High stress conditions generate more signal from each group, perhaps through sensor clustering as proposed for Wsc1 [12, 54]. Extreme stress environment proposes the existence of another pathway, represented here by the question mark, that contributes to the overall stress. The location of this pathway at the plasma membrane was done for convenience and does not imply another cell wall sensor system per se.
320823.fig.007a
(a)
320823.fig.007b
(b)
320823.fig.007c
(c)