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 Previous Article

Molecular and Cellular Biology, February 2003, p. 1470-1476, Vol. 23, No. 4
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.4.1470-1476.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Disruption of the Pelota Gene Causes Early Embryonic Lethality and Defects in Cell Cycle Progression

Ibrahim M. Adham,1* Mahmoud A. Sallam,1 Gerd Steding,2 Monika Korabiowska,3 Ulrich Brinck,3 Sigrid Hoyer-Fender,4 Changkyu Oh,1 and Wolfgang Engel1

Institute of Human Genetics,1 Department of Embryology,2 Department of Cytopathology,3 Department of Zoology and Developmental Biology, University of Göttingen, 37073 Göttingen, Germany4

Received 16 October 2002/ Accepted 6 November 2002

Mutations in either the Drosophila melanogaster pelota or pelo gene or the Saccharomyces cerevisiae homologous gene, DOM34, cause defects of spermatogenesis and oogenesis in Drosophila, and delay of growth and failure of sporulation in yeast. These phenotypes suggest that pelota is required for normal progression of the mitotic and meiotic cell cycle. To determine the role of the pelota in mouse development and progression of cell cycle, we have established a targeted disruption of the mouse Pelo. Heterozygous animals are variable and fertile. Genotyping of the progeny of heterozygous intercrosses shows the absence of Pelo-/- pups and suggests an embryo-lethal phenotype. Histological analyses reveal that the homozygous Pelo deficient embryos fail to develop past day 7.5 of embryogenesis (E7.5). The failure of mitotic active inner cell mass of the Pelo-/- blastocysts to expand in growth after 4 days in culture and the survival of mitotic inactive trophoplast indicate that the lethality of Pelo-null embryos is due to defects in cell proliferation. Analysis of the cellular DNA content reveals the significant increase of aneuploid cells in Pelo-/- embryos at E7.5. Therefore, the percent increase of aneuploid cells at E7.5 may be directly responsible for the arrested development and suggests that Pelo is required for the maintenance of genomic stability.

* Corresponding author. Mailing address: Institut für Humangenetik, Heinrich-Düker-Weg 12, D 37073 Göttingen, Germany. Phone: 49 551 397536. Fax: 49 551 399303. E-mail: iadham{at}gwdg.de.

Molecular and Cellular Biology, February 2003, p. 1470-1476, Vol. 23, No. 4
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.4.1470-1476.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Graille, M., Chaillet, M., van Tilbeurgh, H. (2008). Structure of Yeast Dom34: A PROTEIN RELATED TO TRANSLATION TERMINATION FACTOR Erf1 AND INVOLVED IN No-Go DECAY. J. Biol. Chem. 283: 7145-7154 [Abstract] [Full Text]  
  • Xi, R., Doan, C., Liu, D., Xie, T. (2005). Pelota controls self-renewal of germline stem cells by repressing a Bam-independent differentiation pathway. Development 132: 5365-5374 [Abstract] [Full Text]  


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