Document Detail

Chemical inactivation of cdc7 kinase in budding yeast results in a reversible arrest that allows efficient cell synchronization prior to meiotic recombination.
MedLine Citation:
PMID:  17057233     Owner:  NLM     Status:  MEDLINE    
Genetic studies in budding yeast have provided many fundamental insights into the specialized cell division of meiosis, including the identification of evolutionarily conserved meiosis-specific genes and an understanding of the molecular basis for recombination. Biochemical studies have lagged behind, however, due to the difficulty in obtaining highly synchronized populations of yeast cells. A chemical genetic approach was used to create a novel conditional allele of the highly conserved protein kinase Cdc7 (cdc7-as3) that enables cells to be synchronized immediately prior to recombination. When Cdc7-as3 is inactivated by addition of inhibitor to sporulation medium, cells undergo a delayed premeiotic S phase, then arrest in prophase before double-strand break (DSB) formation. The arrest is easily reversed by removal of the inhibitor, after which cells rapidly and synchronously proceed through recombination and meiosis I. Using the synchrony resulting from the cdc7-as3 system, DSB-dependent phosphorylation of the meiosis-specific chromosomal core protein, Hop1, was shown to occur after DSBs. The cdc7-as3 mutant therefore provides a valuable tool not only for understanding the role of Cdc7 in meiosis, but also for facilitating biochemical and cytological studies of recombination.
Lihong Wan; Chao Zhang; Kevan M Shokat; Nancy M Hollingsworth
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2006-10-22
Journal Detail:
Title:  Genetics     Volume:  174     ISSN:  0016-6731     ISO Abbreviation:  Genetics     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2006-12-21     Completed Date:  2007-02-20     Revised Date:  2013-06-07    
Medline Journal Info:
Nlm Unique ID:  0374636     Medline TA:  Genetics     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1767-74     Citation Subset:  IM    
Department of Biochemistry and Cell Biology, SUNY, Stony Brook, NY 11794-5215, USA.
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MeSH Terms
Cell Cycle Proteins / antagonists & inhibitors,  metabolism*
DNA Breaks, Double-Stranded
DNA Damage
DNA, Fungal / genetics,  metabolism
DNA-Binding Proteins / metabolism
Enzyme Inhibitors / pharmacology
Protein Kinases
Protein-Serine-Threonine Kinases / antagonists & inhibitors,  metabolism*
Recombination, Genetic / genetics*
S Phase / genetics*
Saccharomyces cerevisiae Proteins / antagonists & inhibitors,  metabolism*
Saccharomycetales / genetics*
Grant Support
Reg. No./Substance:
0/Cell Cycle Proteins; 0/DNA, Fungal; 0/DNA-Binding Proteins; 0/Enzyme Inhibitors; 0/HOP1 protein, S cerevisiae; 0/Saccharomyces cerevisiae Proteins; EC 2.7.-/Protein Kinases; EC 2.7.1.-/CDC7 protein, S cerevisiae; EC Kinases

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