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ZFIN ID: ZDB-PUB-080227-5
Completion of meiosis in male zebrafish (Danio rerio) despite lack of DNA mismatch repair gene mlh1
Leal, M.C., Feitsma, H., Cuppen, E., França, L.R., and Schulz, R.W..
Date: 2008
Source: Cell and tissue research   332(1): 133-139 (Journal)
Registered Authors: Cuppen, Edwin, Feitsma, Harma
Keywords: DNA repair enzyme Mlh1, Testis, Spermatogenesis, Male fertility, Aneuploidy, Zebrafish, Danio rerio (Teleostei)
MeSH Terms:
  • Adaptor Proteins, Signal Transducing/genetics*
  • Aneuploidy
  • Animals
  • Animals, Genetically Modified
  • Apoptosis/genetics
  • DNA Mismatch Repair*
  • Embryo, Nonmammalian/metabolism
  • Embryo, Nonmammalian/pathology
  • Female
  • Fertility/genetics
  • Histones/metabolism
  • In Situ Nick-End Labeling
  • Male
  • Meiosis/genetics*
  • Nuclear Proteins/genetics*
  • Organ Size
  • Phenotype
  • Point Mutation
  • Spermatogenesis/genetics*
  • Spermatozoa/metabolism
  • Spermatozoa/pathology
  • Testis/pathology
  • Zebrafish/embryology
  • Zebrafish/genetics*
  • Zebrafish Proteins/genetics*
PubMed: 18247060 Full text @ Cell Tissue Res.
FIGURES
ABSTRACT
Mlh1 is a member of DNA mismatch repair (MMR) machinery and is also essential for the stabilization of crossovers during the first meiotic division. Recently, we have shown that zebrafish mlh1 mutant males are completely infertile because of a block in metaphase I, whereas females are fertile but have aneuploid progeny. When studying fertility in males in a two-fold more inbred background, we have however observed low numbers of fertilized eggs (approximately 0.4%). Histological examination of the testis has revealed that all spermatogenic stages prior to spermatids (spermatogonia, primary spermatocytes, and secondary spermatocytes) are significantly increased in the mutant, whereas the total weight of spermatids and spermatozoa is highly decreased (1.8 mg in wild-type vs. 0.1 mg in mutants), a result clearly different from our previous study in which outbred males lack secondary spermatocytes or postmeiotic cells. Thus, a delay of both meiotic divisions occurs rather than complete arrest during meiosis I in these males. Eggs fertilized with mutant sperm develop as malformed embryos and are aneuploid making this male phenotype much more similar to that previously described in the mutant females. Therefore, crossovers are still essential for proper meiosis, but meiotic cell divisions can progress without it, suggesting that this mutant is a suitable model for studying the cellular mechanisms of completing meiosis without crossover stabilization.
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