Saccharomyces cerevisiae mutants unresponsive to alpha-factor pheromone: alpha-factor binding and extragenic...

Area of Science:

• Molecular Biology
• Genetics
• Cellular Signaling

Background:

• Saccharomyces cerevisiae mating relies on alpha-factor signaling.
• STE genes are crucial for this pheromone response pathway.
• Understanding STE gene function is key to elucidating mating mechanisms.

Purpose of the Study:

• To characterize mutations in six STE genes affecting alpha-factor responsiveness.
• To determine if loss of responsiveness is due to absent alpha-factor receptors.
• To differentiate roles of STE genes in receptor-dependent and post-receptor events.

Main Methods:

• Assaying radioactively labeled alpha-factor binding to yeast cell receptors.
• Analyzing genetic suppression of sterile mutations using sst2-1 and bar1-1.
• Mapping gene positions for STE2, STE12, ROS3, and FUR1.

Main Results:

• ste2 and STE12 mutations abolish alpha-factor receptors, affecting receptor assembly or STE2 mRNA.
• STE4, STE5, STE7, and STE11 mutations partially reduce receptor sites, impacting post-receptor signaling.
• Distinct suppression patterns by sst2-1 and ros1-1 mutations identify two signaling steps, with ste4 mutants affecting both.

Conclusions:

• STE genes regulate alpha-factor response at distinct receptor and post-receptor stages.
• sst2-1 suppresses defects in the STE2-dependent pathway, while ros1-1 suppresses STE5-dependent pathway defects.
• The study provides a refined model for pheromone signal transduction in yeast.