Abstract
In two independent screens we isolated fission yeast mutations with phenotypes suggesting defects ill B-cyclin function or expression. These mutations define a single gene which we call ded1, We show that ded1 encodes a general translation factor that is related in sequence and function to RNA helicases required for translation in other species. Levels of the B-cyclins Cig2 and Cdc13 are dramatically reduced upon inactivation of Ded1, and this reduction is independent of degradation by the anaphase promoting complex. When a ded1 mutant is grown under semi-restrictive conditions, the translation of Cig2 land to a lesser extent Cdc13), is impaired relative to other proteins. We show that B-cyclin translation is specifically inhibited upon nitrogen starvation of wild-type cells, when B-cyclin/Cdc2 inactivation is a prerequisite for G(1) arrest and subsequent mating, Our data suggest that translational inhibition of B-cyclin expression represents a third mechanism, in addition to cyclin degradation and Rum1 inhibition, that contributes to Cdc2 inactivation as cells exit from the mitotic cell cycle and prepare for meiosis.
Original language | English |
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Pages (from-to) | 1447-1458 |
Number of pages | 12 |
Journal | Journal of Cell Science |
Volume | 113 |
Issue number | 8 |
Publication status | Published - 2000 |
Keywords
- MESSENGER-RNAS
- PUTATIVE RNA HELICASE
- translation
- G(1) ARREST
- S-PHASE
- SCHIZOSACCHAROMYCES-POMBE
- POSTERIOR POLE ACCUMULATION
- cell cycle
- B-TYPE CYCLIN
- RNA helicase
- P25(RUM1) CDK INHIBITOR
- B-type cyclin
- DNA-REPLICATION
- ded1
- SACCHAROMYCES-CEREVISIAE