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IME4, a gene that mediates MAT and nutritional control of meiosis in Saccharomyces cerevisiae.

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  • 1. Department of Biological Sciences, University of New Orleans, Louisiana 70148.
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    • Shah JC 1
    (1 author)

Molecular and Cellular Biology, 01 Mar 1992, 12(3):1078-1086
https://doi.org/10.1128/mcb.12.3.1078-1086.1992 PMID: 1545790 PMCID: PMC369539

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Abstract 

In the yeast Saccharomyces cerevisiae, sporulation occurs in response to nutritional and genetic signals. The process is initiated when nutrient availability limits mitotic growth, but only in MATa/MAT alpha diploid cells. Under these conditions, the cells express an activator of meiosis (IME1), which is required for the expression of early sporulation-specific genes. We describe a new gene, IME4, whose activity is essential for IME1 transcript accumulation and sporulation. The IME4 transcript was induced in starved MATa/MAT alpha diploids but not in other cell types. In addition, excess IME4 promoted sporulation in mat-insufficient cells. Thus, IME4 appears to activate IME1 in response to cell type and nutritional signals. We have also explored the interactions between IME4 and two genes that are known to regulate IME1 expression. Normally, cells that lack complete MAT information cannot sporulate; when such strains lack RME1 activity or contain the semidominant RES1-1 mutation, however, they can express IME1 and sporulate to low levels. Our results show that mat-insufficient strains containing rme1::LEU2 or RES1-1 bypass mutations still retain MAT control of IME4 expression. Even though IME4 levels remained low, the rme1::LEU2 and RES1-1 mutations allowed IME1 accumulation, implying that these mutations do not require IME4 to exert their effects. In accord with this interpretation, the RES1-1 mutation allowed IME1 accumulation in MATa/MAT alpha strains that contain ime4::LEU2 alleles. These strains still sporulated poorly, suggesting that IME4 plays a role in sporulation in addition to promoting IME1 transcript accumulation. IME4 is located between ADE5 and LYS5 on chromosome VII.

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Mol Cell Biol. 1992 Mar; 12(3): 1078–1086.
PMCID: PMC369539
PMID: 1545790

IME4, a gene that mediates MAT and nutritional control of meiosis in Saccharomyces cerevisiae.

J C Shah and M J Clancy
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Abstract

In the yeast Saccharomyces cerevisiae, sporulation occurs in response to nutritional and genetic signals. The process is initiated when nutrient availability limits mitotic growth, but only in MATa/MAT alpha diploid cells. Under these conditions, the cells express an activator of meiosis (IME1), which is required for the expression of early sporulation-specific genes. We describe a new gene, IME4, whose activity is essential for IME1 transcript accumulation and sporulation. The IME4 transcript was induced in starved MATa/MAT alpha diploids but not in other cell types. In addition, excess IME4 promoted sporulation in mat-insufficient cells. Thus, IME4 appears to activate IME1 in response to cell type and nutritional signals. We have also explored the interactions between IME4 and two genes that are known to regulate IME1 expression. Normally, cells that lack complete MAT information cannot sporulate; when such strains lack RME1 activity or contain the semidominant RES1-1 mutation, however, they can express IME1 and sporulate to low levels. Our results show that mat-insufficient strains containing rme1::LEU2 or RES1-1 bypass mutations still retain MAT control of IME4 expression. Even though IME4 levels remained low, the rme1::LEU2 and RES1-1 mutations allowed IME1 accumulation, implying that these mutations do not require IME4 to exert their effects. In accord with this interpretation, the RES1-1 mutation allowed IME1 accumulation in MATa/MAT alpha strains that contain ime4::LEU2 alleles. These strains still sporulated poorly, suggesting that IME4 plays a role in sporulation in addition to promoting IME1 transcript accumulation. IME4 is located between ADE5 and LYS5 on chromosome VII.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.
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