Figure S5.
DscIA has antagonistic genetic interactions with CortI and IQGAP1 and synergistic genetic interactions with IQGAP2. (A) Quantification of growth rates during exponential growth in suspension of WT (blue), dsc1 (red) and cortI (green) single mutants, and double mutant (brown) expressing empty plasmids together with their corresponding complemented backgrounds. Expression of DscIA and CortI had opposite effects on growth of cortI; dsc1 double mutant cells. Exogenous expression of DscIA in the absence of CortI was deleterious to growth. Exogenous expression of DscIA rescued the growth defect of dsc1 null, while CortI partially rescued the growth defect of cortI null. Number of cell samples, n = 6 from two independent experiments. (B) Quantification of growth rates during exponential growth in suspension of WT (blue), dsc1 (red) and iqgap1 (orange) single mutants, and double mutant (black) expressing empty plasmids together with their corresponding complemented backgrounds. Exogenous expression of DscIA in the absence of IQGAP1, similar to that of CortI, was also deleterious to growth of iqgap1; dsc1 cells. Exogenous expression of IQGAP1 rescued growth of the double mutant cells. Number of cell samples, n = 6 from two independent experiments. (C) FCCS measurement of in vivo KD values demonstrated that DscIA and IQGAP1 do not detectably interact in the cytoplasm in either the WT or in the iqgap1; dsc1 complemented backgrounds. Positive and negative controls (shaded) in WT background are reproduced from Fig. 7 C. Compared to the negative control, the P values of the interactions in the WT background was 0.64 and in the iqgap1; dsc1-complemented background was 0.16. P values were derived from an ANOVA followed by Fisher’s LSD test. Number of cells analyzed, n = 10–30 from two independent experiments. (D) Quantification of growth rates during exponential growth in suspension of WT (blue), dsc1 (red) and iqgap2 (purple) single mutants, and double mutant (gray) expressing empty plasmids together with their corresponding complemented backgrounds. Exogenous expression of DscIA and IQGAP2 rescued the growth of iqgap2; dsc1 double mutant cells, returning growth to the single mutant levels. All growth rate values in these experiments are detailed in Table S2. All P values were derived by ANOVA followed by Fisher’s LSD test (*, P < 0.05; **, P < 0.001; ***, P < 0.0001). Number of cell samples, n = 6 from two independent experiments.

DscIA has antagonistic genetic interactions with CortI and IQGAP1 and synergistic genetic interactions with IQGAP2. (A) Quantification of growth rates during exponential growth in suspension of WT (blue), dsc1 (red) and cortI (green) single mutants, and double mutant (brown) expressing empty plasmids together with their corresponding complemented backgrounds. Expression of DscIA and CortI had opposite effects on growth of cortI; dsc1 double mutant cells. Exogenous expression of DscIA in the absence of CortI was deleterious to growth. Exogenous expression of DscIA rescued the growth defect of dsc1 null, while CortI partially rescued the growth defect of cortI null. Number of cell samples, n = 6 from two independent experiments. (B) Quantification of growth rates during exponential growth in suspension of WT (blue), dsc1 (red) and iqgap1 (orange) single mutants, and double mutant (black) expressing empty plasmids together with their corresponding complemented backgrounds. Exogenous expression of DscIA in the absence of IQGAP1, similar to that of CortI, was also deleterious to growth of iqgap1; dsc1 cells. Exogenous expression of IQGAP1 rescued growth of the double mutant cells. Number of cell samples, n = 6 from two independent experiments. (C) FCCS measurement of in vivo KD values demonstrated that DscIA and IQGAP1 do not detectably interact in the cytoplasm in either the WT or in the iqgap1; dsc1 complemented backgrounds. Positive and negative controls (shaded) in WT background are reproduced from Fig. 7 C. Compared to the negative control, the P values of the interactions in the WT background was 0.64 and in the iqgap1; dsc1-complemented background was 0.16. P values were derived from an ANOVA followed by Fisher’s LSD test. Number of cells analyzed, n = 10–30 from two independent experiments. (D) Quantification of growth rates during exponential growth in suspension of WT (blue), dsc1 (red) and iqgap2 (purple) single mutants, and double mutant (gray) expressing empty plasmids together with their corresponding complemented backgrounds. Exogenous expression of DscIA and IQGAP2 rescued the growth of iqgap2; dsc1 double mutant cells, returning growth to the single mutant levels. All growth rate values in these experiments are detailed in Table S2. All P values were derived by ANOVA followed by Fisher’s LSD test (*, P < 0.05; **, P < 0.001; ***, P < 0.0001). Number of cell samples, n = 6 from two independent experiments.

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