Cytoplasmic Clb2 is required for timely inactivation of the mitotic inhibitor Swe1 and normal bud morphogenesis in Saccharomyces cerevisiae

2006 ◽  
Vol 51 (1) ◽  
pp. 1-18 ◽  
Author(s):  
Jennifer K. Hood-DeGrenier ◽  
Cortney N. Boulton ◽  
Victoria Lyo
1982 ◽  
Vol 2 (9) ◽  
pp. 1064-1079
Author(s):  
J S Wood

The genetic effects of the mitotic inhibitor methyl benzimidazole-2-yl-carbamate (MBC) have been studied in Saccharomyces cerevisiae. MBC had little or no effect on the frequency of mutation. In some experiments MBC caused an increase in the frequency of mitotic recombination; however, this effect was small and not reproducible. The primary genetic effect of MBC was to induce mitotic chromosome loss at a high frequency. Chromosome loss occurred at equal frequencies for all chromosomes tested (13 of 16). Cells which had lost multiple chromosomes were found more frequently than predicted if individual chromosome loss events were independent. The probability of loss for a particular chromosome increased with length of time cells were incubated with MBC. MBC treatment also increased the frequency at which polyploid cells were found. These results suggested that MBC acted to disrupt the structure or function of the mitotic spindle and cause chromosome nondisjunction.


2016 ◽  
Vol 27 (11) ◽  
pp. 1764-1775 ◽  
Author(s):  
Hui Kang ◽  
Denis Tsygankov ◽  
Daniel J. Lew

Bud formation by Saccharomyces cerevisiae must be coordinated with the nuclear cycle to enable successful proliferation. Many environmental stresses temporarily disrupt bud formation, and in such circumstances, the morphogenesis checkpoint halts nuclear division until bud formation can resume. Bud emergence is essential for degradation of the mitotic inhibitor, Swe1. Swe1 is localized to the septin cytoskeleton at the bud neck by the Swe1-binding protein Hsl7. Neck localization of Swe1 is required for Swe1 degradation. Although septins form a ring at the presumptive bud site before bud emergence, Hsl7 is not recruited to the septins until after bud emergence, suggesting that septins and/or Hsl7 respond to a “bud sensor.” Here we show that recruitment of Hsl7 to the septin ring depends on a combination of two septin-binding kinases: Hsl1 and Elm1. We elucidate which domains of these kinases are needed and show that artificial targeting of those domains suffices to recruit Hsl7 to septin rings even in unbudded cells. Moreover, recruitment of Elm1 is responsive to bud emergence. Our findings suggest that Elm1 plays a key role in sensing bud emergence.


2008 ◽  
Vol 19 (11) ◽  
pp. 4675-4686 ◽  
Author(s):  
Lee Szkotnicki ◽  
John M. Crutchley ◽  
Trevin R. Zyla ◽  
Elaine S.G. Bardes ◽  
Daniel J. Lew

Saccharomyces cerevisiae cells growing in the outdoor environment must adapt to sudden changes in temperature and other variables. Many such changes trigger stress responses that delay bud emergence until the cells can adapt. In such circumstances, the morphogenesis checkpoint delays mitosis until a bud has been formed. Mitotic delay is due to the Wee1 family mitotic inhibitor Swe1p, whose degradation is linked to bud emergence by the checkpoint kinase Hsl1p. Hsl1p is concentrated at the mother-bud neck through association with septin filaments, and it was reported that Hsl1p activation involved relief of autoinhibition in response to septin interaction. Here we challenge the previous identification of an autoinhibitory domain and show instead that Hsl1p activation involves the phosphorylation of threonine 273, promoted by the septin-associated kinase Elm1p. We identified elm1 mutants in a screen for defects in Swe1p degradation and show that a phosphomimic T273E mutation in HSL1 bypasses the need for Elm1p in this pathway.


1982 ◽  
Vol 2 (9) ◽  
pp. 1064-1079 ◽  
Author(s):  
J S Wood

The genetic effects of the mitotic inhibitor methyl benzimidazole-2-yl-carbamate (MBC) have been studied in Saccharomyces cerevisiae. MBC had little or no effect on the frequency of mutation. In some experiments MBC caused an increase in the frequency of mitotic recombination; however, this effect was small and not reproducible. The primary genetic effect of MBC was to induce mitotic chromosome loss at a high frequency. Chromosome loss occurred at equal frequencies for all chromosomes tested (13 of 16). Cells which had lost multiple chromosomes were found more frequently than predicted if individual chromosome loss events were independent. The probability of loss for a particular chromosome increased with length of time cells were incubated with MBC. MBC treatment also increased the frequency at which polyploid cells were found. These results suggested that MBC acted to disrupt the structure or function of the mitotic spindle and cause chromosome nondisjunction.


2001 ◽  
Vol 36 (2) ◽  
pp. 196-201 ◽  
Author(s):  
F. Seibold ◽  
O. Stich ◽  
R. Hufnagl ◽  
S. Kamil ◽  
M. Scheurlen

Planta Medica ◽  
2016 ◽  
Vol 81 (S 01) ◽  
pp. S1-S381
Author(s):  
N Grčić ◽  
R Oliveira ◽  
ACP Dias

2007 ◽  
Vol 45 (08) ◽  
Author(s):  
S Schmechel ◽  
V Schachinger ◽  
F Seibold ◽  
C Tillack ◽  
T Ochsenkühn ◽  
...  

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