NDD1, a high-dosage suppressor of cdc28-1N, is essential for expression ofa subset of late-S-phase-specific genes in Saccharomyces cerevisiae

Citation
Cj. Loy et al., NDD1, a high-dosage suppressor of cdc28-1N, is essential for expression ofa subset of late-S-phase-specific genes in Saccharomyces cerevisiae, MOL CELL B, 19(5), 1999, pp. 3312-3327
Citations number
58
Categorie Soggetti
Molecular Biology & Genetics
Journal title
MOLECULAR AND CELLULAR BIOLOGY
ISSN journal
02707306 → ACNP
Volume
19
Issue
5
Year of publication
1999
Pages
3312 - 3327
Database
ISI
SICI code
0270-7306(199905)19:5<3312:NAHSOC>2.0.ZU;2-C
Abstract
cdc28-1N mutants progress through the G(1) and S phases normally at the res trictive temperature but fail to undergo nuclear division. We have isolated a gene, NDD1, which at a high dosage suppresses the nuclear-division defec t of cdc28-1N. NDD1 (nuclear division defective) is an essential gene. Its expression during the cell cycle is tightly regulated such that NDD1 RNA is most abundant during the S phase, Cells lacking the NDD1 gene arrest with an elongated bud, a short mitotic spindle, 2N DNA content, and an undivided nucleus, suggesting that Its function is required for some aspect of nucle ar division. We show that overexpression of Ndd1 results in the upregulatio n of both CLB1 and CLB2 transcription, suggesting that the suppression of c dc28-1N by NDD1 may be due to an accumulation of these cyclins. Overproduct ion of Ndd1 also enhances the expression of SWI5, whose transcription, like that of CLB1 and CLB2, is activated in the late S phase. Ndd1 is essential for the expression of CLB1, CLB2, and SWI5, since none of these genes are transcribed in its absence. Both CLB2 expression and its upregulation by ND D1 are mediated by a 240-bp promoter sequence that contains four MCM1-bindi ng sites. However, Ndd1 does not appear to be a component of any of the pro tein complexes assembled on this DNA fragment, as indicated by gel mobility shift assays. Instead, overexpression of NDD1 prevents the formation of on e of the complexes whose appearance correlates with the termination of CLB2 expression in G(1), The inability of GAL1 promoter-driven CLB2 to suppress the lethality of NDD1 null mutant suggests that, in addition to CLB1 and C LB2, NDDI may also be required for the transcription of other genes whose f unctions are necessary for G(2)/M transition.