Transcriptional regulation of meiosis in budding yeast
Transcriptional regulation of meiosis in budding yeast
Transcriptional regulation of meiosis in budding yeast
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(L<strong>in</strong>dgren et al., 2000). S<strong>in</strong>ce Ime2 mediates the availability <strong>of</strong> Sum1 under normal meiotic<br />
conditions, it is possible that the effect <strong>of</strong> the checkpo<strong>in</strong>t system on Sum1 is mediated through<br />
Ime2. Pak and Segall (Pak and Segall, 2002b) suggest that the effect <strong>of</strong> Sum1 is mediated only<br />
through regulat<strong>in</strong>g the transcription <strong>of</strong> NDT80, s<strong>in</strong>ce the triple mutant dmc1 sum1 ndt80 does not<br />
enter nuclear division (Pak and Segall, 2002b). Morovere, they propose that <strong>in</strong> the dmc1 sum1<br />
cells, expression <strong>of</strong> the B-type cycl<strong>in</strong>s is responsible for entry <strong>in</strong>to meiotic nuclear division (Pak<br />
and Segall, 2002b). This hypothesis is supported by the observation that entry <strong>in</strong>to nuclear<br />
division <strong>in</strong> swe1 hop2 cells is delayed <strong>in</strong> comparison to wild type cells or to swe1 hop2 cells over<br />
express<strong>in</strong>g Clb1 (Leu and Roeder, 1999). However, this model cannot expla<strong>in</strong> why ectopic<br />
expression <strong>of</strong> Ndt80 <strong>in</strong> dmc1 cells leads to <strong>in</strong>efficient entry <strong>in</strong>to nuclear division <strong>in</strong> comparison to<br />
the dmc1 sum1 cells (20% versus 60%) (Pak and Segall, 2002b). These results suggest that an<br />
additional target <strong>of</strong> Sum1 might be required for proper meiotic arrest (L<strong>in</strong>dgren et al., 2000).<br />
S<strong>in</strong>ce the CLB genes are not direct targets <strong>of</strong> Sum1, they are not the genes directly regulated by<br />
Sum1 (L<strong>in</strong>dgren et al., 2000).<br />
The pachytene checkpo<strong>in</strong>t <strong>in</strong>hibits phosphorylation <strong>of</strong> Ntd80 (Tung et al., 2000). In cells<br />
deleted for ZIP1 [a component <strong>of</strong> the synaptonemal complex required for synapsis <strong>of</strong> homologs<br />
(Sym et al., 1993)] Ndt80 is partially phosphorylated (Tung et al., 2000), whereas <strong>in</strong> the double<br />
mutants zip1 pch2 and zip1 mek1 it is highly phosphorylated (Tung et al., 2000). It was suggested<br />
that activation <strong>of</strong> transcription by Ndt80 requires its phosphorylation (Benjam<strong>in</strong> et al., 2002; Chu<br />
and Herskowitz, 1998; Hepworth et al., 1998; Tung et al., 2000). Therefore, lack <strong>of</strong> expression <strong>of</strong><br />
MMG is also due to the reduction <strong>in</strong> the phosphorylation <strong>of</strong> Ndt80. S<strong>in</strong>ce Ime2 is required for<br />
phosphorylation <strong>of</strong> Ndt80, it should be <strong>in</strong>terest<strong>in</strong>g to determ<strong>in</strong>e if Ime2 is the target for the<br />
pachytene check po<strong>in</strong>t system.<br />
In addition, the pachytene checkpo<strong>in</strong>t mediates the transcription <strong>of</strong> MMG through the Cdc28<br />
<strong>in</strong>hibitor, Swe1. In swe1 hop2 diploid cells CLB1 transcription is <strong>in</strong>creased to its normal level,<br />
although with a substantial delay, <strong>in</strong> comparison to wild type or hop2 cells (Leu and Roeder,<br />
1999). It should be <strong>in</strong>terest<strong>in</strong>g to determ<strong>in</strong>e whether this effect <strong>of</strong> Swe1 on Cdc28 is mediated<br />
through Ime2, s<strong>in</strong>ce Cdc28 is required for the activity <strong>of</strong> Ime2 that co<strong>in</strong>cides with nuclear<br />
divisions (Benjam<strong>in</strong> et al., 2002), and Ime2 is absolutely required for the transcription <strong>of</strong> the CLB<br />
genes.<br />
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