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A Genetic Screen for Saccharomyces cerevisiae Mutants That Fail to Enter Quiescence.

Li L, Miles S, Breeden LL - G3 (Bethesda) (2015)

Bottom Line: They undergo asymmetric cell divisions, slow cellular expansion, acquire significant stress tolerance and construct elaborate cell walls.Acquired thermotolerance is also a common property, and we show that the stress-response transcription factors Msn2 and Msn4 promote quiescence.Many other pathways also contribute, including a subset of genes involved in autophagy, ubiquitin-mediated proteolysis, DNA replication, bud site selection, and cytokinesis.

View Article: PubMed Central - PubMed

Affiliation: Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109.

No MeSH data available.


Related in: MedlinePlus

DNA fluorescence histograms of R3-deficient (Rtd−) mutants after 24 hr of growth in rich glucose medium. The first two histograms (WT1 and WT2) reflect the extent of variation we observe with wild-type cells.
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fig3: DNA fluorescence histograms of R3-deficient (Rtd−) mutants after 24 hr of growth in rich glucose medium. The first two histograms (WT1 and WT2) reflect the extent of variation we observe with wild-type cells.

Mentions: If there is a unique conformation of R3 DNA, we might identify mutants that influence that process. We also expect to find mutants that fail in the upstream recognition and/or signaling events that initiate the transition to quiescence. There may be other mutants that are unable to cope with the stresses that arise during this metabolic transition. Such defects could lead to slow growth, death, or a checkpoint arrest, any of which could delay, obscure, or prevent the processes that lead to R3 cell formation. With this in mind, we screened the deletion library of nonessential genes (Tong et al. 2001) for Rtd− mutants. Here, we report the identification of 118 mutants that produce little or no R3 cells (Table 1). Parentheses indicate Rtd− mutants that are adjacent to another Rtd− mutant. In these cases, it is possible that the Rtd− phenotype shared by adjacent genes is conferred by loss of only one of the genes, but the disruption of the adjacent gene interferes with transcription of its neighbor (Alvaro et al. 2007). For example, there is a cluster of four Rtd− mutants (YHL042W to YHL046C) that are unlikely to all be required to form R3 cells (Table 1). In this case, it may be that disruption of one or more of these loci is interfering with the transcription of one gene in the cluster that is conferring the Rtd− phenotype. This has been referred to as neighboring gene effect (Ben-Shitrit et al. 2012). Representative DNA fluorescence histograms of all 118 Rtd− mutants are shown in Figure 3.


A Genetic Screen for Saccharomyces cerevisiae Mutants That Fail to Enter Quiescence.

Li L, Miles S, Breeden LL - G3 (Bethesda) (2015)

DNA fluorescence histograms of R3-deficient (Rtd−) mutants after 24 hr of growth in rich glucose medium. The first two histograms (WT1 and WT2) reflect the extent of variation we observe with wild-type cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4528334&req=5

fig3: DNA fluorescence histograms of R3-deficient (Rtd−) mutants after 24 hr of growth in rich glucose medium. The first two histograms (WT1 and WT2) reflect the extent of variation we observe with wild-type cells.
Mentions: If there is a unique conformation of R3 DNA, we might identify mutants that influence that process. We also expect to find mutants that fail in the upstream recognition and/or signaling events that initiate the transition to quiescence. There may be other mutants that are unable to cope with the stresses that arise during this metabolic transition. Such defects could lead to slow growth, death, or a checkpoint arrest, any of which could delay, obscure, or prevent the processes that lead to R3 cell formation. With this in mind, we screened the deletion library of nonessential genes (Tong et al. 2001) for Rtd− mutants. Here, we report the identification of 118 mutants that produce little or no R3 cells (Table 1). Parentheses indicate Rtd− mutants that are adjacent to another Rtd− mutant. In these cases, it is possible that the Rtd− phenotype shared by adjacent genes is conferred by loss of only one of the genes, but the disruption of the adjacent gene interferes with transcription of its neighbor (Alvaro et al. 2007). For example, there is a cluster of four Rtd− mutants (YHL042W to YHL046C) that are unlikely to all be required to form R3 cells (Table 1). In this case, it may be that disruption of one or more of these loci is interfering with the transcription of one gene in the cluster that is conferring the Rtd− phenotype. This has been referred to as neighboring gene effect (Ben-Shitrit et al. 2012). Representative DNA fluorescence histograms of all 118 Rtd− mutants are shown in Figure 3.

Bottom Line: They undergo asymmetric cell divisions, slow cellular expansion, acquire significant stress tolerance and construct elaborate cell walls.Acquired thermotolerance is also a common property, and we show that the stress-response transcription factors Msn2 and Msn4 promote quiescence.Many other pathways also contribute, including a subset of genes involved in autophagy, ubiquitin-mediated proteolysis, DNA replication, bud site selection, and cytokinesis.

View Article: PubMed Central - PubMed

Affiliation: Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109.

No MeSH data available.


Related in: MedlinePlus