Transcriptional regulation of meiosis in budding yeast

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(Lindgren et al., 2000). Since Ime2 mediates the availability of Sum1 under normal meiotic conditions, it is possible that the effect of the checkpoint system on Sum1 is mediated through Ime2. Pak and Segall (Pak and Segall, 2002b) suggest that the effect of Sum1 is mediated only through regulating the transcription of NDT80, since the triple mutant dmc1 sum1 ndt80 does not enter nuclear division (Pak and Segall, 2002b). Morovere, they propose that in the dmc1 sum1 cells, expression of the B-type cyclins is responsible for entry into meiotic nuclear division (Pak and Segall, 2002b). This hypothesis is supported by the observation that entry into nuclear division in swe1 hop2 cells is delayed in comparison to wild type cells or to swe1 hop2 cells over expressing Clb1 (Leu and Roeder, 1999). However, this model cannot explain why ectopic expression of Ndt80 in dmc1 cells leads to inefficient entry into nuclear division in comparison to the dmc1 sum1 cells (20% versus 60%) (Pak and Segall, 2002b). These results suggest that an additional target of Sum1 might be required for proper meiotic arrest (Lindgren et al., 2000). Since the CLB genes are not direct targets of Sum1, they are not the genes directly regulated by Sum1 (Lindgren et al., 2000). The pachytene checkpoint inhibits phosphorylation of Ntd80 (Tung et al., 2000). In cells deleted for ZIP1 [a component of the synaptonemal complex required for synapsis of homologs (Sym et al., 1993)] Ndt80 is partially phosphorylated (Tung et al., 2000), whereas in the double mutants zip1 pch2 and zip1 mek1 it is highly phosphorylated (Tung et al., 2000). It was suggested that activation of transcription by Ndt80 requires its phosphorylation (Benjamin et al., 2002; Chu and Herskowitz, 1998; Hepworth et al., 1998; Tung et al., 2000). Therefore, lack of expression of MMG is also due to the reduction in the phosphorylation of Ndt80. Since Ime2 is required for phosphorylation of Ndt80, it should be interesting to determine if Ime2 is the target for the pachytene check point system. In addition, the pachytene checkpoint mediates the transcription of MMG through the Cdc28 inhibitor, Swe1. In swe1 hop2 diploid cells CLB1 transcription is increased to its normal level, although with a substantial delay, in comparison to wild type or hop2 cells (Leu and Roeder, 1999). It should be interesting to determine whether this effect of Swe1 on Cdc28 is mediated through Ime2, since Cdc28 is required for the activity of Ime2 that coincides with nuclear divisions (Benjamin et al., 2002), and Ime2 is absolutely required for the transcription of the CLB genes. 37
VI. Transcriptional regulation of late meiosis-specific genes A. Early late genes. SGA1 is an early-late gene encoding a glucoamylase whose transcription in growth media is silenced by a negative element, NRE SGA , which exhibits no UAS activity (Kihara et al., 1991; Mai and Breeden, 2000). Expression under meiotic conditions depends on a UAS element present in its promoter region (Kihara et al., 1991). In addition, it carries 4 STRE elements (Mai and Breeden, 2000), but their role in the transcription of SGA1 is not known. Relief of repression by the NRE SGA element depends on Ime1 and Ime2. However, the activity of the UAS element is independent of these regulators, because it does not require the presence of both MATa and MATα alleles that are required for the expression of Ime1 (Kihara et al., 1991). The activity of the positive element requires nitrogen depletion (Kihara et al., 1991), demonstrating that the effect of nitrogen on meiosis is mediated not only through Ime1. Silencing of SGA1 in vegetative growth media depends on the chromatin-remodeling factor Isw2 (Goldmark et al., 2000). As described above (section IVA5), Isw2 is also a negative regulator of EMG, and it is recruited by Ume6 to their promoters. Since the URS1 element to which Ume6 binds is not present in SGA1, it is not known how Isw2 is recruited to SGA1. The identities of the positive regulators promoting transcriptional activation of SGA1 are not known. However, one positive regulator, SME2, when present on a multi-copy plasmid, increases the transcription of SGA1 in the presence of nitrogen, thus bypassing also the nitrogen signal inhibiting spore formation (Kawaguchi et al., 1992). Deletion of SME2 has no effect on the regulated expression of SGA1, or on the efficiency of sporulation. The sequence and mode of function of SME2 are not known. B. Mid-late genes. The transcription of the mid-late sporulation-specific genes DIT1 and DIT2 is induced upon completion of meiotic divisions (Friesen et al., 1997). Time of expression is compatible with function, since these divergently transcribed genes (Friesen et al., 1997) encode enzymes required for biosynthesis of the dityrosine precursor that is incorporated into the outermost layer of the spore wall (Briza et al., 1990). A negative element, designated NRE DIT is required for repression during vegetative growth (Friesen et al., 1997) (Note that NRE DIT is not identical to NRE SGA1 ). This region carries the middle sporulation-like element MSE, and the DRE element (Bogengruber et al., 1998; Friesen et al., 1997) that are required for repression in growth conditions and activation under meiotic conditions. Two additional positive elements are required for high expression under meiotic conditions (Friesen et al., 1997). 38
Page 1 and 2: Transcriptional regulation of meios
Page 3 and 4: 3. Proteins required for the associ
Page 5 and 6: I. Introduction The budding yeast S
Page 7 and 8: et al., 2000). On the other hand, i
Page 9 and 10: the UCS4 element upstream of the CY
Page 11 and 12: egulator of Cyr1, CDC25 encodes the
Page 13 and 14: 1998). Furthermore, unlike IREu, IR
Page 15 and 16: In the absence of glucose Sok2 does
Page 17 and 18: autophosphorylation, including on a
Page 19 and 20: hours in SPM, followed by a decline
Page 21 and 22: 4. The SIN3, UME6, and RPD3 genes.
Page 23 and 24: 1993). Nevertheless, when Ime1 is t
Page 25 and 26: However, direct demonstration of ph
Page 27 and 28: 3. Proteins required for the associ
Page 29 and 30: heterologous promoter does not supp
Page 31 and 32: expressed only in the absence of gl
Page 33 and 34: structure of hCDK2 reveals that cyc
Page 35 and 36: terminal non-essential domain (Komi
Page 37: is dependent on Ime2, but in cells
Page 41 and 42: The transcriptional activator that
Page 43 and 44: Functional interaction between Ime1
Page 45 and 46: Bowdish, K. S., and Mitchell, A. P.
Page 47 and 48: Foiani, M., Nadjar-Boger, E., Capon
Page 49 and 50: Jeffrey, P. D., Russo, A. A., Polya
Page 51 and 52: Lindgren, A., Bungard, D., Pierce,
Page 53 and 54: Pazin, M. J., and Kadonaga, J. T. (
Page 55 and 56: Shenhar, G. (2001). TRANSCRIPTIONAL
Page 57 and 58: Szent-Gyorgyi, C. (1995). A biparti
Page 59 and 60: Yoshida, M., Kawaguchi, H., Sakata,
Page 61 and 62: Fig. 4. The function of positive an
Page 63 and 64: Fig. 9. A schematic structure of IM
Page 65 and 66: activation by Ime2 is due to phosph
Page 67 and 68: MCK1 Protein kinase required for ef
Page 69: UME3 A cyclin C homolog that associ

Transcriptional regulation of meiosis in budding yeast

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