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doi: 10.1242/10.1242/dev.00385

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Development 130, 1605-1620 (2003)
Copyright © 2003 The Company of Biologists Limited

Developmental defects observed in hypomorphic anaphase-promoting complex mutants are linked to cell cycle abnormalities

Diane C. Shakes1,*,{dagger}, Penny L. Sadler2,*, Jill M. Schumacher3, Maziar Abdolrasulnia1 and Andy Golden2

1 Department of Biology, College of William and Mary, Williamsburg, Virginia 23187, USA
2 Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
3 Department of Molecular Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030 and Genes and Development Program, Graduate School of Biomedical Sciences, The University of Texas-Houston, Houston, TX 77030, USA

{dagger} Author for correspondence (e-mail: dcshak{at}wm.edu)

Accepted 9 January 2003

In C. elegans, mutants in the anaphase-promoting complex or cyclosome (APC/C) exhibit defects in germline proliferation, the formation of the vulva and male tail, and the metaphase to anaphase transition of meiosis I. Oocytes lacking APC/C activity can be fertilized but arrest in metaphase of meiosis I and are blocked from further development. To examine the cell cycle and developmental consequences of reducing but not fully depleting APC/C activity, we analyzed defects in embryos and larvae of mat-1/cdc-27 mutants grown at semi-permissive temperatures. Hypomorphic embryos developed to the multicellular stage but were slow to complete meiosis I and displayed aberrant meiotic chromosome separation. More severely affected embryos skipped meiosis II altogether and exhibited striking defects in meiotic exit. These latter embryos failed to produce normal eggshells or establish normal asymmetries prior to the first mitotic division. In developing larvae, extended M-phase delays in late-dividing cell lineages were associated with defects in the morphogenesis of the male tail. This study reveals the importance of dosage-specific mutants in analyzing molecular functions of a ubiquitously functioning protein within different cell types and tissues, and striking correlations between specific abnormalities in cell cycle progression and particular developmental defects.

Key words: mat-1/cdc-27, Asymmetric cell divisions, Meiosis, Cell cycle, APC/C, Caenorhabditis elegans




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