In two independent screens we isolated fission yeast mutations with phenotypes suggesting defects in 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 (and 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.
A fission yeast general translation factor reveals links between protein synthesis and cell cycle controls
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B. Grallert, S.E. Kearsey, M. Lenhard, C.R. Carlson, P. Nurse, E. Boye, K. Labib; A fission yeast general translation factor reveals links between protein synthesis and cell cycle controls. J Cell Sci 15 April 2000; 113 (8): 1447–1458. doi: https://doi.org/10.1242/jcs.113.8.1447
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