Latham K E, Doherty A S, Scott C D, Schultz R M
Temple University School of Medicine, Department of Biochemistry, Philadelphia, Pennsylvania 19140.
Genes Dev. 1994 Feb 1;8(3):290-9. 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.
哺乳动物中的基因组印记被认为是配子发生过程中染色体修饰的结果，这种修饰会使父本或母本等位基因失活。在胎儿和成年小鼠中，编码胰岛素样生长因子2（Igf2）及其受体（Igf2r）的基因相互印记，分别从父本和母本基因组表达。我们发现这两个基因在孤雄生殖、孤雌生殖和孤雌激活的植入前小鼠胚胎中均有表达。这些结果表明，印记基因的失活发生在受精后（很可能是植入后），并且基因组印记和基因失活是两个独立的过程。我们提出，印记标记了染色体，以便后期细胞中表达的调节因子能够识别印记并选择性地使母本或父本等位基因失活。对于这些基因，这一发现使那些要求它们从受精时起就处于失活状态的基因组印记模型无效。
