XXXX mutants unresponsive to alpha-factor pheromone: alpha-factor binding and extragenic suppression.

@entity33372 @entity71025 @entity6771 @entity5679 @entity5678 @entity71023 @entity71024 @entity9457 @entity25220 @entity375 @entity71026
Mutations in six genes that eliminate responsiveness of @entity375 a cells to alpha-factor were examined by assaying the binding of radioactively labeled alpha-factor to determine whether their lack of responsiveness was due to the absence of alpha-factor receptors. The @entity25220 mutants, known to be defective in the structural gene for the receptor, were found to lack receptors when grown at the restrictive temperature; these mutations probably affect the assembly of active receptors. Mutations in @entity9457 known to block @entity25220 mRNA accumulation also resulted in an absence of receptors. Mutations in @entity5679 , 5, 7, and 11 partially reduced the number of binding sites, but this reduction was not sufficient to explain the loss of responsiveness; the products of these genes appear to affect postreceptor steps of the response pathway. As a second method of distinguishing the roles of the various STE genes, we examined the sterile mutants for suppression. Mating of the @entity71023 mutant was apparently limited by its sensitivity to alpha-factor, as its sterility was suppressed by mutation @entity33372 -1, which leads to enhanced alpha-factor sensitivity. Sterility resulting from each of four @entity5679 mutations was suppressed partially by mutation @entity33372 -1 or by mutation bar1-1 when one of three other mutations ( @entity71024 -1, ros2-1, or @entity71025 -1) was also present. Sterility of the @entity5678 -3 mutant was suppressed by mutation @entity71024 -1 but not by @entity33372 -1. The @entity6771 , 11, and 12 mutations were not suppressed by @entity71024 or @entity33372 . Our working model is that STE genes control the response to alpha-factor at two distinct steps. Defects at one step (requiring the @entity25220 gene are suppressed (directly or indirectly) by mutation @entity33372 -1, whereas defects at the other step (requiring the @entity5678 gene) are suppressed by the @entity71024 -1 mutation. The @entity5679 mutants are defective for both steps. Mutation @entity71024 -1 was found to be allelic to cdc39-1. Map positions for genes @entity25220 , @entity9457 , @entity71025 , and @entity71026 were determined.
