2006
DOI: 10.1016/j.cub.2005.11.070
|View full text |Cite|
|
Sign up to set email alerts
|

The Conserved Kinases CDK-1, GSK-3, KIN-19, and MBK-2 Promote OMA-1 Destruction to Regulate the Oocyte-to-Embryo Transition in C. elegans

Abstract: Our findings suggest that a CDK1/Cyclin B3-dependent activity links OMA-1 proteolysis to completion of the first cell cycle and support a model in which OMA-1 functions to prevent the premature activation of cell-fate determinants until after they are asymmetrically partitioned during the first mitosis.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
2

Citation Types

4
104
1
1

Year Published

2010
2010
2023
2023

Publication Types

Select...
5
1

Relationship

1
5

Authors

Journals

citations
Cited by 96 publications
(110 citation statements)
references
References 39 publications
(64 reference statements)
4
104
1
1
Order By: Relevance
“…17,18 However, the phenotypes exhibited by these mutants were not simply caused by defects in cell cycle progression; for both mutants, the striking defects observed in cell fate specification occur in embryos that show an otherwise wild-type pattern and timing of cell division. 16 Consistent with these findings, when immunoprecipitated from embryonic lysates CDK-1(ne2257) was shown to phosphorylate Histone H1, a well-known CDK1 substrate during mitosis, at levels similar to that observed for wild-type CDK-1. 16 These observations suggest that the function of cdk-1 in cell fate specification can be uncoupled from its role in driving progression through the cell cycle.…”
Section: Cell Fate Specification Regulated By C Elegans Cdk1supporting
confidence: 62%
See 4 more Smart Citations
“…17,18 However, the phenotypes exhibited by these mutants were not simply caused by defects in cell cycle progression; for both mutants, the striking defects observed in cell fate specification occur in embryos that show an otherwise wild-type pattern and timing of cell division. 16 Consistent with these findings, when immunoprecipitated from embryonic lysates CDK-1(ne2257) was shown to phosphorylate Histone H1, a well-known CDK1 substrate during mitosis, at levels similar to that observed for wild-type CDK-1. 16 These observations suggest that the function of cdk-1 in cell fate specification can be uncoupled from its role in driving progression through the cell cycle.…”
Section: Cell Fate Specification Regulated By C Elegans Cdk1supporting
confidence: 62%
“…16 Consistent with these findings, when immunoprecipitated from embryonic lysates CDK-1(ne2257) was shown to phosphorylate Histone H1, a well-known CDK1 substrate during mitosis, at levels similar to that observed for wild-type CDK-1. 16 These observations suggest that the function of cdk-1 in cell fate specification can be uncoupled from its role in driving progression through the cell cycle.…”
Section: Cell Fate Specification Regulated By C Elegans Cdk1supporting
confidence: 62%
See 3 more Smart Citations