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Comparison of Gene Expression During Preimplantation Development Between Diploid and Haploid Mouse Embryos¹

^a The Fels Institute for Cancer Research and Molecular Biology and ^b The Department of Biochemistry, Temple University School of Medicine, Philadelphia, Pennsylvania 19140 ^c Institute for Biogenesis Research, The John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii 96822

Haploid development is a normal part of the life cycle for some animals, but it has not been observed in mammals. Studies in mice have revealed that the preimplantation developmental potential of haploid embryos is significantly impaired relative to diploid embryos. The reasons for the severely limited developmental potential of haploid embryos in mammals have not been discerned. To examine the effects of haploid development on gene expression, and in particular on X-linked gene expression, and to evaluate to what degree newer techniques of producing and culturing such embryos might affect developmental potential, haploid and diploid parthenogenetic and androgenetic embryos were produced and reevaluated for developmental potential, genomic integrity, and relative expression levels of specific autosomal and X-linked gene transcripts. Our data confirm the previously observed restriction in haploid developmental potential, eliminate chromosomal abnormalities as a major factor in this restriction, and reveal subtle alterations in gene expression. Haploid parthenogenones display only very subtle alterations in the expression of most mRNAs but a consistent elevation in X-linked Bex1 mRNA expression. Haploid androgenones seem to lack repression of the Pgk1 gene that is seen in diploid androgenones, but this may reflect ongoing loss of those haploid androgenones that experience X chromosome inactivation. The significance and possible explanations for these differences are discussed.

First decision: 3 December 2001.

¹ Supported in parts by grants from the NIH (RR15253), the Harold K. Castle Foundation, and the Victoria and Bradley Geist Foundation.

² Correspondence: Keith E. Latham, The Fels Institute for Cancer Research, Temple University School of Medicine, 3307 North Broad St., Philadelphia, PA 19140. FAX: 215 707 1454; klatham{at}unix.temple.edu

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