A network of transcription factors (TFs) coordinates transcription with cell cycle events in eukaryotes. Most TFs in the network are phosphorylated by cyclin-dependent kinase (CDK), which limits their activities during the cell cycle. Here, we investigate the physiological consequences of disrupting CDK regulation of the paralogous repressors Yhp1 and Yox1 in yeast. Blocking Yhp1/Yox1 phosphorylation increases their levels and decreases expression of essential cell cycle regulatory genes which, unexpectedly, increases cellular fitness in optimal growth conditions. Using synthetic genetic interaction screens, we find that Yhp1/Yox1 mutations improve the fitness of mutants with mitotic defects, including condensin mutants. Blocking Yhp1/Yox1 phosphorylation simultaneously accelerates the G1/S transition and delays mitotic exit, without decreasing proliferation rate. This mitotic delay partially reverses the chromosome segregation defect of condensin mutants, potentially explaining their increased fitness when combined with Yhp1/Yox1 phosphomutants. These findings reveal how altering expression of cell cycle genes leads to a redistribution of cell cycle timing and confers a fitness advantage to cells.
Her research mainly focused on the study of the proteomic profile of extracellular vesicles and the secretome in virulent and avirulent strains of Candida albicans. She continued her scientific carrier at the University of Massachusetts Medical School working on yeast genetics and proteomics. Her current research at the Forsyth Institute affiliated with Harvard School of Dental Medicine is focused on understanding how the organic matrix composition of enamel is affected by the oral environment in healthy and defective teeth. She has authored peer-reviewed research articles, reviews, and has presented her work to national and international scientific meetings.
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