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Updated: Jul 26, 2026
Computational Analysis of the Caenorhabditis elegans Germline to Study the Distribution of Nuclei, Proteins, and the Cytoskeleton
Published on: April 19, 2018
Metaphase to anaphase (mat) transition-defective mutants in Caenorhabditis elegans
A Golden1, P L Sadler, M R Wallenfang
1Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Abstract:
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.
Insights
Researchers identified 32 "mat" mutants in C. elegans that cause embryonic lethality due to defects in the metaphase to anaphase transition, impacting cell cycle progression and chromosome segregation.
Area of Science:
- Cell Biology
- Genetics
- Developmental Biology
Background:
- The transition from metaphase to anaphase is a critical, highly regulated cell cycle stage.
- Errors in this transition can cause chromosome segregation defects and organismal death.
Purpose of the Study:
- To identify and characterize mutants with defects in the metaphase to anaphase transition in C. elegans.
- To investigate the genetic basis of cell cycle regulation and its impact on embryonic development.
Main Methods:
- Conducted genetic screens for temperature-sensitive maternal effect embryonic lethal (Mel) mutants in C. elegans.
- Analyzed embryonic and germline cell cycle progression, including meiosis and mitosis.
- Mapped identified mutants to genes encoding subunits of the anaphase promoting complex/cyclosome.
Main Results:
- Identified 32 "mat" (metaphase to anaphase transition defective) mutants exhibiting one-cell embryonic arrest.
- Observed metaphase I arrest in oocytes and spermatocytes, failure to produce polar bodies, and M phase exit blocks.
- Demonstrated that the emb-27 gene encodes the C. elegans CDC16 ortholog, a subunit of the anaphase promoting complex.
Conclusions:
- The identified "mat" mutants are crucial for understanding the regulation of the metaphase to anaphase transition.
- Defects in the anaphase promoting complex/cyclosome lead to severe cell cycle arrest and embryonic lethality.
- emb-27 is essential for proper cell cycle progression in C. elegans meiosis and mitosis.
