Nutritional Regulation of Meiosis-specific Gene Expression in <i>Saccharomyces cerevisiae</i>

Kawaguchi, Haruko; Yoshida, Manabu; Yamashita, Ichiro

doi:10.1271/bbb.56.289

Cited by 33 publications

(29 citation statements)

References 8 publications

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“…4B), which is consistent with elevated expression of IME1 in cells grown on nonfermentable carbon sources (Fig. 8E) and after exponential growth on glucose (44). The pseudohyphal growth defect of the T99N-Ume6-expressing cells was also not as severe as the pseudohyphal growth defect displayed by ime1⌬/ime1⌬ cells, either because of a residual interaction between T99N-Ume6 and Ime1 or because of the existence of additional, Ume6-independent Ime1 targets.…”

Section: Discussionsupporting

confidence: 79%

Ime1 and Ime2 Are Required for Pseudohyphal Growth of Saccharomyces cerevisiae on Nonfermentable Carbon Sources

Strudwick

Brown

Parmar

et al. 2010

Molecular and Cellular Biology

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Pseudohyphal growth and meiosis are two differentiation responses to nitrogen starvation of diploid Saccharomyces cerevisiae. Nitrogen starvation in the presence of fermentable carbon sources is thought to induce pseudohyphal growth, whereas nitrogen and sugar starvation induces meiosis. In contrast to the genetic background routinely used to study pseudohyphal growth (⌺1278b), nonfermentable carbon sources stimulate pseudohyphal growth in the efficiently sporulating strain SK1. Pseudohyphal SK1 cells can exit pseudohyphal growth to complete meiosis. Two stimulators of meiosis, Ime1 and Ime2, are required for pseudohyphal growth of SK1 cells in the presence of nonfermentable carbon sources. Epistasis analysis suggests that Ime1 and Ime2 act in the same order in pseudohyphal growth as in meiosis. The different behaviors of strains SK1 and ⌺1278b are in part attributable to differences in cyclic AMP (cAMP) signaling. In contrast to ⌺1278b cells, hyperactivation of cAMP signaling using constitutively active Ras2 G19V inhibited pseudohyphal growth in SK1 cells. Our data identify the SK1 genetic background as an alternative genetic background for the study of pseudohyphal growth and suggest an overlap between signaling pathways controlling pseudohyphal growth and meiosis. Based on these findings, we propose to include exit from pseudohyphal growth and entry into meiosis in the life cycle of S. cerevisiae.

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Section: Discussionsupporting

confidence: 79%

Ime1 and Ime2 Are Required for Pseudohyphal Growth of Saccharomyces cerevisiae on Nonfermentable Carbon Sources

Strudwick

Brown

Parmar

et al. 2010

Molecular and Cellular Biology

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“…The T 4 C site is not required for URS1 to respond to IME1; rather, the T 4 C site amplifies the IME1-dependent activation signal. In addition, the T 4 C site may be responsible for glucose repression of IME2, which is independent of IME1 expression (8).…”

Section: Discussionmentioning

confidence: 99%

Positive Control of Yeast Meiotic Genes by the Negative Regulator UME6

Bowdish

Yuan

Mitchell

1995

Molecular and Cellular Biology

104

141

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The yeast meiotic activator IME1 stimulates transcription of many early meiotic genes. These genes share a 5 sequence called URS1. URS1 sites function as repression sites in cells that lack IME1; we show here that URS1 sites are weak activation sequences in cells that express IME1. Repression through URS1 sites is known to depend upon the URS1-binding protein UME6. We have identified a UME6 allele (previously called rim16-12) that causes a defect in IME1-dependent activation of meiotic genes but not in repression through URS1 sites. In contrast, a ume6 null mutation causes defects in both IME1-dependent activation and in repression through URS1 sites. A LexA-UME6 fusion protein is an IME1-dependent transcriptional activator, whereas a LexA-UME6 fusion carrying the rim16-12 substitution cannot activate transcription. These findings argue that IME1 activates meiotic genes by converting UME6 from a negative regulator to a positive regulator; the rim16-12 mutant protein is defective in conversion to a positive regulator.The yeast UME6 protein and URS1 site are components of a sequence-specific repression system. URS1 sites are widely distributed in genetic regulatory regions (29), where they function as repression sites in growing, nonmeiotic cells (4,10,12,17,31). Repression of URS1-containing genes requires the UME6 gene product (16,27). UME6 is a zinc cluster protein that binds specifically to a URS1 site in vitro (27). A second protein, the RPA1/2/3 heterotrimer (RP-A), also binds to URS1 sites (11). Binding of RP-A is independent of UME6 (16), and binding of recombinant UME6 is independent of RP-A (27). The functional relationship among RP-A, URS1, and other URS1-binding proteins is presently unclear. However, genetic analysis indicates that UME6 is a repressor or part of a repression complex that acts through URS1 sites in nonmeiotic cells (16,27).Three observations made in nonmeiotic cells indicate that the URS1/UME6 system participates in repression of early meiotic genes. First, URS1-like sites are found upstream of almost all early meiotic genes (4; see reference 14 for a compilation). Second, mutations that remove or disrupt these URS1 sites cause increased expression in nonmeiotic cells (1,4,31). Third, ume6 loss-of-function mutations cause increased early meiotic gene expression in nonmeiotic cells (1,26,27). Thus, repression by the URS1/UME6 system prevents inappropriate meiotic gene expression in nonmeiotic cells.Entry into meiosis is accompanied by elevated expression of IME1 (7); the IME1 gene product is required for expression of almost all meiotic genes (see reference 14 for a review). Two observations indicate that the URS1/UME6 system may be required for IME1 to activate early meiotic genes. First, mutations in the URS1 sites near the meiotic genes SPO13, HOP1, and IME2 cause reduced expression during meiosis (1,4,31). At HOP1 and IME2, mutations in nearby positive sites (called the UAS H [UAS, upstream activating sequence] and T 4 C sites) also cause reduced expression during meiosis (1, 31). S...

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“…RNA blot analysis was carried out as described (Kawaguchi et al, 1992;Yoshida et al, 1990;Hayashi et al, 1998b), except using as probes a 0.45 kb EcoRI±HindIII fragment of CLN3, 1.23 kb AatI±SacII of SRB10, 0.59 kb BglII±HindIII of SRB11, 1.53 kb HindIII±BamHI of CCR4, 0.82 kb KIN28, 1.03 kb CCL1, 1.91 kb SSA4 and 0.65 kb CUP1. The fragments of KIN28, CCL1, SSA4, and CUP1 lie in open reading frames and were obtained through PCR ampli®cation with primer pairs as follows: KIN28 (5k-GTTGGTGAGGGTACTTAT-GC-3k and 5k-CTAAACACTGAACAGCGGTC-3k); CCL1 (5k-ACTCCTTCTGCTACCATGTC-3k and 5k-TCTTGGCCTCTTCAGTACTC-3k); SSA4 (5k-GGCCTATCTCTTCTTTCTCC-3k and 5k-AT-GGGGTTTGCAACACCTTC-3k); and CUP1 (5k-CTGTCAGTCACTGTCAAGAG-3k and 5k-ATT-CTTGGGGCGACATATGG-3k).…”

Section: Rna Blot Analysismentioning

confidence: 99%

A transcriptional autoregulatory loop for KIN28–CCL1 and SRB10–SRB11, each encoding RNA polymerase II CTD kinase–cyclin pair, stimulates the meiotic development of S. cerevisiae

Ohkuni¹,

Yamashita²

2000

Yeast

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Alkalization of the medium is associated with and required for the cellular development to meiosis and sporulation in the yeast Saccharomyces cerevisiae. To elucidate the molecular mechanisms for the signi®cance of external alkalization, we isolated mutants defective in division arrest at G 1 phase under an alkaline condition. The mutants obtained had recessive alleles of SRB10 encoding the cyclin (SRB11)-dependent protein kinase that phosphorylates the CTD domain of the largest subunit of RNA polymerase II and negatively regulates the transcriptional initiation of certain genes. A Dsrb11 deletion mutant showed the same cell cycle defect. When shifted to alkali, wild-type cells decreased transcript levels of G 1 -cyclin genes (CLN1 to CLN3) and KIN28±CCL1 (encoding another CTD kinase±cyclin pair which, in contrast, stimulates the promoter clearance and transcriptional elongation in most genes), resulting in the accumulation of G 1 cells and the hypophosphorylated form of RNA polymerase II and in an increase in cell size. However, under the same conditions, a Dsrb10 mutant was defective in these events, except the downregulation of CLN1 and CLN2. The Dsrb10 mutation also in¯uenced on the transcript levels of meiosis-inducing genes called IME1 and IME2: the mutation elevated the transcript level of IME1 but reduced that of IME2, resulting in partial defects in premeiotic DNA synthesis and meiosis. Overexpression of KIN28 and CCL1 in wild-type cells impaired the alkali-induced G 1 arrest and the rate of meiosis and elevated the transcript levels of SRB11 and IME1. These results indicate that a transcriptional autoregulatory loop for KIN28±CCL1 and SRB10±SRB11 is important for G 1 arrest and meiosis. We also found that environmental conditions for meiosis ®nely regulate the transcript levels of KIN28 and CCL1, such that nitrogen starvation ®rst elevates them but subsequent alkalization of medium decreases them.

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Nutritional Regulation of Meiosis-specific Gene Expression in Saccharomyces cerevisiae

Cited by 33 publications

References 8 publications

Ime1 and Ime2 Are Required for Pseudohyphal Growth of Saccharomyces cerevisiae on Nonfermentable Carbon Sources

Ime1 and Ime2 Are Required for Pseudohyphal Growth of Saccharomyces cerevisiae on Nonfermentable Carbon Sources

Positive Control of Yeast Meiotic Genes by the Negative Regulator UME6

A transcriptional autoregulatory loop for KIN28–CCL1 and SRB10–SRB11, each encoding RNA polymerase II CTD kinase–cyclin pair, stimulates the meiotic development of S. cerevisiae

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