Figure 3.
Figure 3. Septation mutant viability requires Fir1 to prevent inappropriate Cts1 secretion. (A) Loss of FIR1 is detrimental to cells with septation defects. Fivefold serial dilutions of the indicated strains were spotted to YPD media as in Fig. 1 C (see also Fig. S2 B). (B) CTS1 deletion rescues the lethality of inn1-AID fir1Δ. Fivefold serial dilutions of the indicated strains were spotted to YPD as in Fig. 1 C. (C) CTS1 transcript induction is not altered by lack of FIR1. CTS1 mRNA from cells in D were measured by qPCR as in Fig. 2 A. A representative time course from two independent experiments is shown. (D) Fir1 blocks Cts1 secretion when septation fails. inn1-AID fir1Δ cells expressing HA-tagged Cts1 were synchronized in mitosis and treated with DMSO (−Auxin) or 0.5 mM auxin (+Auxin). Cells were collected and processed as in Fig. 2 B. (E) Western blot quantification (as in Fig. 2 C; Fig. 3, C–E, was done in parallel with Fig. 2, A–C).

Septation mutant viability requires Fir1 to prevent inappropriate Cts1 secretion. (A) Loss of FIR1 is detrimental to cells with septation defects. Fivefold serial dilutions of the indicated strains were spotted to YPD media as in Fig. 1 C (see also Fig. S2 B). (B) CTS1 deletion rescues the lethality of inn1-AID fir1Δ. Fivefold serial dilutions of the indicated strains were spotted to YPD as in Fig. 1 C. (C) CTS1 transcript induction is not altered by lack of FIR1. CTS1 mRNA from cells in D were measured by qPCR as in Fig. 2 A. A representative time course from two independent experiments is shown. (D) Fir1 blocks Cts1 secretion when septation fails. inn1-AID fir1Δ cells expressing HA-tagged Cts1 were synchronized in mitosis and treated with DMSO (−Auxin) or 0.5 mM auxin (+Auxin). Cells were collected and processed as in Fig. 2 B. (E) Western blot quantification (as in Fig. 2 C; Fig. 3, C–E, was done in parallel with Fig. 2, A–C).

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