Comparison of gene expression during preimplantation development between diploid and haploid mouse embryos.
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.
The Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, 3307 North Broad Street, Philadelphia, PA 19140, USA. klatham@unix.temple.edu
Keith E
KE
Latham
Hidenori
H
Akutsu
Bela
B
Patel
Ryuzo
R
Yanagimachi
D000818:Animals; D001755:Blastocyst / Q000502:physiology*; D002869:Chromosome Aberrations; D003470:Culture Media; D004171:Diploidy; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000235:genetics / Q000502:physiology*; D006238:Haploidy; D017403:In Situ Hybridization; D007202:Indicators and Reagents; D051379:Mice; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D010312:Parthenogenesis / Q000502:physiology; D011247:Pregnancy; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014960:X Chromosome / Q000235:genetics
D003470:Culture Media; D007202:Indicators and Reagents; D012333:RNA, Messenger