Abstract
The polarized partitioning of proteins in cells underlies asymmetric cell division, which is an important driver of development and cellular diversity. The budding yeast Saccharomyces cerevisiae divides asymmetrically, like many other cells, to generate two distinct progeny cells. A well-known example of an asymmetric protein is the transcription factor Ace2, which localizes specifically to the daughter nucleus, where it drives a daughter-specific transcriptional network. We screened a collection of essential genes to analyze the effects of core cellular processes in asymmetric cell division based on Ace2 localization. This screen identified mutations that affect progression through the cell cycle, suggesting that cell cycle delay is sufficient to disrupt Ace2 asymmetry. To test this model, we blocked cells from progressing through mitosis and found that prolonged metaphase delay is sufficient to disrupt Ace2 asymmetry after release, and that Ace2 asymmetry is restored after cytokinesis. We also demonstrate that members of the evolutionarily conserved facilitates chromatin transcription (FACT) chromatin-reorganizing complex are required for both asymmetric and cell cycle-regulated localization of Ace2, and for localization of the RAM network components.
Highlights
IntroductionThe budding yeast Saccharomyces cerevisiae divides asymmetrically to give two distinct daughter cells
Abstract which is an important driver of development and cellular diversity
We have systematically screened a collection of ts mutants of essential genes for those that perturb the asymmetry of a canonical marker of asymmetric cell fate determination, Ace2 (Fig. 1)
Summary
The budding yeast Saccharomyces cerevisiae divides asymmetrically to give two distinct daughter cells This asymmetry mimics that seen in metazoans and the key regulatory proteins are conserved from yeast to human. We screened a collection of essential genes in order to analyze the effect of core cellular processes in asymmetric cell division This identified a large number of mutations that are known to affect progression through the cell cycle, suggesting that cell cycle delay is sufficient to disrupt Ace asymmetry. Asymmetric cell division utilizes the polarity axis of the cell to align the mitotic spindle such that the plane of cell division is perpendicular to the axis of cell polarity In this way, polarized proteins are partitioned differentially into the two daughter cells, potentially altering their fates (Neumuller and Knoblich, 2009). Identifying the mechanisms driving the asymmetric proteins distribution via cell polarity is fundamentally important to understand stem cell function and cell fate determination
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