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Published online 25 December 2000. doi:10.1083/jcb.151.7.1469
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© The Rockefeller University Press, 0021-9525/2000//1469 $5.00
The Journal of Cell Biology, Volume 151, Number 7, , 2000 1469-1482

Original Article

Metaphase to Anaphase (mat) Transition–Defective Mutants inCaenorhabditis elegans



Andy Goldena, Penny L. Sadlerb,c, Matthew R. Wallenfangd, Jill M. Schumachere, Danielle R. Hamillf, Gayle Batesc, Bruce Bowermanf, Geraldine Seydouxd, and Diane C. Shakesc

a Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892
b Department of Biology, University of Houston, Houston, Texas 77204
c Department of Biology, College of William and Mary, Williamsburg, Virginia 23187
d Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205
e Department of Molecular Genetics, University of Texas, M.D. Anderson Cancer Center, Houston, Texas 77030
f Institute of Molecular Biology, University of Oregon, Eugene, Oregon 97403
Department of Biology, College of William and Mary, P.O. Box 8795, Williamsburg, VA 23187.(757) 221-6483(757) 221-2409

dcshak{at}wm.edu

The metaphase to anaphase transition is a critical stage of the eukaryotic cell cycle, and, thus, it is highly regulated. Errors during this transition can lead to chromosome segregation defects and death of the organism. In genetic screens for temperature-sensitive maternal effect embryonic lethal (Mel) mutants, we have identified 32 mutants in the nematode Caenorhabditis elegans in which fertilized embryos arrest as one-cell embryos. In these mutant embryos, the oocyte chromosomes arrest in metaphase of meiosis I without transitioning to anaphase or producing polar bodies. An additional block in M phase exit is evidenced by the failure to form pronuclei and the persistence of phosphohistone H3 and MPM-2 antibody staining. Spermatocyte meiosis is also perturbed; primary spermatocytes arrest in metaphase of meiosis I and fail to produce secondary spermatocytes. Analogous mitotic defects cause M phase delays in mitotic germline proliferation. We have named this class of mutants "mat" for metaphase to anaphase transition defective. These mutants, representing six different complementation groups, all map near genes that encode subunits of the anaphase promoting complex or cyclosome, and, here, we show that one of the genes, emb-27, encodes the C. elegans CDC16 ortholog.

Key Words: meiosis • metaphase arrest • cell cycle • C. elegans • anaphase promoting complex

© 2000 Government

A. Golden and P.L. Sadler contributed equally to this work.

Abbreviations used in this paper: APC/C, anaphase promoting complex or cyclosome; CDK, cyclin-dependent kinase; DAPI, 4,6-diamidino-2-phenylindole; DIC, differential interference contrast; Mel, maternal effect embryonic lethal; RNAi, RNA-mediated interference; Ste, sterile; TPR, tetratricopeptide repeat; ts, temperature sensitive.


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