Igf2r and Igf2 gene expression in androgenetic, gynogenetic, and parthenogenetic preimplantation mouse embryos : absence of regulation by genomic imprinting

• Published in: Genes & development Vol. 8; no. 3; pp. 290 - 299
• Main Authors: LATHAM, K. E, DOHERTY, A. S, SCOTT, C. D, SCHULTZ, R. M
• Format: Journal Article
• Language: English
• Published: Cold Spring Harbor, NY Cold Spring Harbor Laboratory 01.02.1994
• Subjects: Alleles; Animals; Biological and medical sciences; Blastocyst; Cleavage Stage, Ovum; Embryonic and Fetal Development - genetics; Fathers; Female; Fundamental and applied biological sciences. Psychology; Gene expression; Gene Expression Regulation; Gestational Age; Insulin-Like Growth Factor II - genetics; Male; Methylation; Mice; Molecular and cellular biology; Molecular genetics; Morula; Mothers; Parthenogenesis - genetics; Polymerase Chain Reaction; Receptors, Somatomedin - genetics; RNA, Messenger - analysis; Sex Factors; Time Factors; Embryo; Rodentia; Blastocyst; Gene expression; Insulin like growth factor 2; Genomic imprinting; Vertebrata; Regulation(control); Mammalia; Mouse; Polypeptide; Development; Growth factor; Biological receptor
• ISSN: 0890-9369; 1549-5477
• DOI: 10.1101/gad.8.3.290

Genomic imprinting in mammals is believed to result from modifications to chromosomes during gametogenesis that inactivate the paternal or maternal allele. The genes encoding the insulin-like growth factor type 2 (Igf2) and its receptor (Igf2r) are reciprocally imprinted and expressed from the paternal and maternal genomes, respectively, in the fetal and adult mouse. We find that both genes are expressed in androgenetic, gynogenetic, and parthenogenetic preimplantation mouse embryos. These results indicate that inactivation of imprinted genes occurs postfertilization (most likely postimplantation) and that genomic imprinting and gene inactivation are separate processes. We propose that imprinting marks the chromosome so that regulatory factors expressed in cells at later times can recognize the imprint and selectively inactivate the maternal or paternal allele. For these genes, this finding invalidates models of genomic imprinting that require them to be inactive from the time of fertilization.