Effects of X chromosome number and parental origin on X-linked gene expression in preimplantation mouse embryos.
Diploid androgenetic mouse embryos, possessing two sets of paternally inherited chromosomes, and control fertilized embryos were used to examine the relative effects of X chromosome number and parental chromosome origin on androgenone viability and X-linked gene expression. A significant difference in efficiency of blastocyst formation was observed between XX and XY androgenones in some experiments, but this difference was not uniformly observed. Significant effects of both X chromosome number and parental origin on X-linked gene expression were observed. Male and female control embryos expressed the XIST: RNA initially. This expression was followed by a preferential reduction in XIST: RNA abundance in male embryos, indicating that dosage compensation for the X chromosome may normally require the downregulation of XIST: RNA expression in male embryos, in conjunction with the production of stable XIST: transcripts in female embryos. By the late blastocyst stage, XX control embryos expressed significantly more XIST: RNA than did XY embryos. Unlike their normal counterparts, XX androgenones did not express significantly more XIST: RNA than did XY androgenones at the late blastocyst stage. Androgenones exhibited severe repression of the Pgk1 gene, but during development to the late blastocyst stage Pgk1 mRNA expression increased in XX androgenones and decreased in XY androgenones. Thus, the initial repression of the Pgk1 gene in XX androgenones was lost as the XIST: RNA declined in abundance, and this loss was correlated with a failure of XX androgenones to express significantly more XIST: RNA than did XY androgenones. These results indicate that androgenones may lack a factor that is expressed from the maternal genome and required for dosage compensation in preimplantation embryos. The results also indicate that early dosage compensation in preimplantation embryos may normally be reversible, thus providing flexibility to meet different developmental requirements of the embryonic and extraembryonic lineages.
Latham
K E
KE
The Fels Institute for Cancer Research and Molecular Biology and Department of Biochemistry, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA. klatham@astro.ocis.temple.edu
Patel
B
B
Bautista
F D
FD
Hawes
S M
SM
D000818:Animals; D001755:Blastocyst / Q000502:physiology; D004303:Dosage Compensation, Genetic; D004622:Embryo, Mammalian / Q000502:physiology*; D047108:Embryonic Development / Q000235:genetics*; D005260:Female; D015870:Gene Expression; D008040:Genetic Linkage; D018392:Genomic Imprinting; D007041:Hypoxanthine Phosphoribosyltransferase / Q000235:genetics; D008297:Male; D051379:Mice; D008806:Mice, Inbred AKR; D008810:Mice, Inbred C57BL; D010735:Phosphoglycerate Kinase / Q000235:genetics; D011247:Pregnancy; D030481:Pyruvate Dehydrogenase (Lipoamide); D011768:Pyruvate Dehydrogenase Complex / Q000235:genetics; D062085:RNA, Long Noncoding; D012333:RNA, Messenger; D022661:RNA, Untranslated; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D012268:Ribose-Phosphate Pyrophosphokinase / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics; D014960:X Chromosome
D011768:Pyruvate Dehydrogenase Complex; D062085:RNA, Long Noncoding; D012333:RNA, Messenger; D022661:RNA, Untranslated; D014157:Transcription Factors; C077885:XIST non-coding RNA; D030481:Pyruvate Dehydrogenase (Lipoamide); C065640:pyruvate dehydrogenase E1alpha subunit; D007041:Hypoxanthine Phosphoribosyltransferase; D010735:Phosphoglycerate Kinase; D012268:Ribose-Phosphate Pyrophosphokinase