The Ste16 WD-repeat protein regulates cell-cycle progression under starvation through the Rum1 protein in Schizosaccharomyces pombe

1998 ◽  
Vol 33 (1) ◽  
pp. 29-37 ◽  
Author(s):  
Hiromi Maekawa ◽  
Kenji Kitamura ◽  
C. Shimoda
Keyword(s):  
Cell Cycle ◽  
Schizosaccharomyces Pombe ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Repeat Protein ◽  
Wd Repeat

scholarly journals The role of proteolysis in cell cycle progression in Schizosaccharomyces pombe.

1996 ◽  
Vol 15 (19) ◽  
pp. 5268-5279 ◽  
Author(s):  
H. Yamano ◽  
J. Gannon ◽  
T. Hunt
Keyword(s):  
Cell Cycle ◽  
Schizosaccharomyces Pombe ◽  
Cell Cycle Progression ◽  
Cycle Progression

Vertebrate p34cdc2 phosphorylation site mutants: effects upon cell cycle progression in the fission yeast Schizosaccharomyces pombe

1992 ◽  
Vol 102 (1) ◽  
pp. 43-53 ◽  
Author(s):  
W. Krek ◽  
J. Marks ◽  
N. Schmitz ◽  
E.A. Nigg ◽  
V. Simanis
Keyword(s):  
Cell Cycle ◽  
Schizosaccharomyces Pombe ◽  
Cell Cycle Arrest ◽  
Fission Yeast ◽  
Cell Cycle Progression ◽  
Atp Binding ◽  
In Vitro Mutagenesis ◽  
Cycle Progression ◽  
Cycle Arrest ◽  
P34 Cdc2

We have used the fission yeast Schizosaccharomyces pombe to analyse the effects of in vitro mutagenesis of the four known phosphorylation sites in the chicken p34(cdc2) protein, Thr 14, Tyr 15, Thr 161 and Ser 277, upon cell cycle progression. We have studied both the effect of overexpression of mutant proteins in a cdc2+ background and assayed their ability to rescue null and temperature-sensitive alleles of cdc2. Mutations of Thr 14 and Tyr 15 within the ATP binding domain of p34(cdc2) that mimic constitutive phosphorylation cause dominant negative cell cycle arrest when overexpressed. In contrast, some substitutions that simulate permanent dephosphorylation of the corresponding sites advance dephosphorylation of the corresponding sites advance mitosis. These data confirm the model that p34(cdc2) function is negatively regulated by phosphorylation of residues in the ATP binding site. Mutagenesis of the conserved residue Thr 161 functionally inactivates p34(cdc2), and our data suggest that both phosphorylation and dephosphorylation events at Thr 161 are required for progression through the cell cycle. Mutations at the fourth site of phosphorylation. Ser 277, lead to cold-sensitive cell cycle arrest, in minimal but not rich growth medium, suggesting that this site is involved in monitoring the nutritional status of the cell.

The C. elegans F-box/WD-repeat protein LIN-23 functions to limit cell division during development

Development ◽  
2000 ◽  
Vol 127 (23) ◽  
pp. 5071-5082 ◽  
Author(s):  
E.T. Kipreos ◽  
S.P. Gohel ◽  
E.M. Hedgecock
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Cycle Progression ◽  
Cell Cycle Regulators ◽  
Loss Of Function ◽  
Repeat Protein ◽  
C Elegans ◽  
Blast Cells ◽  
Wd Repeat ◽  
And Function

In multicellular eukaryotes, a complex program of developmental signals regulates cell growth and division by controlling the synthesis, activation and degradation of G(1) cell cycle regulators. Here we describe the lin-23 gene of Caenorhabditis elegans, which is required to restrain cell proliferation in response to developmental cues. In lin-23 null mutants, all postembryonic blast cells undergo extra divisions, creating supernumerary cells that can differentiate and function normally. In contrast to the inability to regulate the extent of blast cell division in lin-23 mutants, the timing of initial cell cycle entry of blast cells is not affected. lin-23 encodes an F-box/WD-repeat protein that is orthologous to the Saccharomyces cerevisiae gene MET30, the Drosophila melanogaster gene slmb and the human gene betaTRCP, all of which function as components of SCF ubiquitin-ligase complexes. Loss of function of the Drosophila slmb gene causes the growth of ectopic appendages in a non-cell autonomous manner. In contrast, lin-23 functions cell autonomously to negatively regulate cell cycle progression, thereby allowing cell cycle exit in response to developmental signals.

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