Ume3p/Srb11p represses the transcription of genes required for
the stress response and meiosis. To relieve this repression, Ume3p is
rapidly destroyed in cells exposed to heat shock or during meiosis. This
present study found that Ume3p is also destroyed in cells subjected to
oxidative stress, ethanol shock and carbon starvation but not osmotic
shock, UV irradiation or nitrogen deprivation. Ume3p levels are also
reduced in cultures growing on a non-fermentable carbon source (e.g.
acetate). Of the three destruction signals (cyclin box, RxxL, PEST)
required for Ume3p heat-induced degradation, only the cyclin box is
involved in its destruction in response to these additional stresses.
However, the PEST domain is required for reducing Ume3p levels during
acetate growth. These findings indicate that Ume3p is controlled though
multiple regulatory pathways. Using an in vivo recruitment assay,
two rut mutations (for r egulator of U me3p
t urnover) were identified that cause a 3-6 fold increase in Ume3p
half-life in response to heat shock. Phenotypic analysis revealed that
MAT a rut1 mutants are unable to mate most likely
due to the derepression of the HML silent mating cassette.
Rut2 strains mate normally but are unable to complete meiosis and
make spores. Examination of DAPI stained cells revealed that a majority
of the rut2 cells remain mono-nucleated suggesting the block
occurs prior to the first meiotic division. Moreover, the nuclei in
cells that had undergone at least one division appear mis-segregated
and/or fragmented. The results indicate that in addition to controlling
Ume3p, RUT1 and RUT2 also regulate key aspects of cell
type specification and meiotic development.
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