Figure 2.

Exomer is not a component of the cell integrity pathway (CIP). (a) Schematic representation of the order of action of the CIP components analysed in this work. (b) Analysis of the viable in immunosuppressant and chloride (VIC) phenotype in the indicated strains. 3 × 10⁴ cells and serial 1:4 dilutions were plated on YES and YES with 1 μg ml⁻¹ of FK506 and 0.2 M MgCl₂ plates. The plates were incubated at 32°C for 2 days. (c) CIP activity in the wild-type control (WT) and the cfr1Δ or the bch1Δ mutants growing in YES medium. The activation was analysed in purified Pmk1-HA:6His samples by western blot using anti-p42/44 (phosphorylated Pmk1) and anti-HA (total Pmk1) antibodies. (d) The same as in (c), but using the WT and pmp1Δ, cfr1Δ and cfr1Δ pmp1Δ strains treated with 0.6 M of KCl for the indicated times. (e) The same as in (d), but using the WT, cfr1Δ, pek1-S234D,T238D (pek1DD) and cfr1Δ pek1DD strains. In (c–e), the bar graphs depicted below the blots represent the CIP activity, calculated as the ratio between the p42/44 (phosphorylated Pmk1) and HA (total Pmk1) signals. They show the mean and standard deviation. a.u., arbitrary units. The t‐test and Tukey correction after ANOVA were used to determine the statistical significance of the differences in (c) and in (d,e), respectively. ns, non-significant; *p < 0.05; ***p < 0.001; ****p < 0.0001.