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Molecular and Cellular Biology, July 2000, p. 4838-4848, Vol. 20, No. 13
Howard Hughes Medical
Institute,2 Department of Molecular,
Cellular, and Developmental Biology,1 and
Department of Genetics,3 Yale
University, New Haven, Connecticut 06520-8103
Received 17 December 1999/Returned for modification 4 February
2000/Accepted 6 April 2000
The Saccharomyces cerevisiae zip1 mutant, which
exhibits defects in synaptonemal complex formation and meiotic
recombination, triggers a checkpoint that causes cells to arrest at the
pachytene stage of meiotic prophase. Overproduction of either the
meiotic chromosomal protein Red1 or the meiotic kinase Mek1 bypasses
this checkpoint, allowing zip1 cells to sporulate.
Red1 or Mek1 overproduction also promotes sporulation of other mutants
(zip2, dmc1, hop2) that undergo
checkpoint-mediated arrest at pachytene. In addition, Red1
overproduction antagonizes interhomolog interactions in the zip1 mutant, substantially decreasing double-strand break
formation, meiotic recombination, and homologous chromosome pairing.
Mek1 overproduction, in contrast, suppresses checkpoint-induced arrest without significantly decreasing meiotic recombination.
Cooverproduction of Red1 and Mek1 fails to bypass the checkpoint;
moreover, overproduction of the meiotic chromosomal protein Hop1 blocks
the Red1 and Mek1 overproduction phenotypes. These results suggest that
meiotic chromosomal proteins function in the signaling of meiotic
prophase defects and that the correct stoichiometry of Red1, Mek1, and Hop1 is needed to achieve checkpoint-mediated cell cycle arrest at pachytene.
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Bypass of a Meiotic Checkpoint by Overproduction
of Meiotic Chromosomal Proteins
and
*
Corresponding author. Mailing address: Howard Hughes
Medical Institute, Department of Molecular, Cellular, and Developmental Biology, Yale University, P.O. Box 208103, New Haven, CT 06520-8103. Phone: (203) 432-3501. Fax: (203) 432-3263. E-mail:
shirleen.roeder{at}yale.edu.
Present address: deCODE Genetics, Inc., 110 Reykjavik, Iceland.
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