Smith F M, Garfield A S, Ward A
Centre for Regenerative Medicine and Developmental Biology Programme, Department of Biology and Biochemistry, University of Bath, Bath, UK.
Cytogenet Genome Res. 2006;113(1-4):279-91. doi: 10.1159/000090843.
A small sub-set of mammalian genes are subject to regulation by genomic imprinting such that only one parental allele is active in at least some sites of expression. Imprinted genes have diverse functions, notably including the regulation of growth. Much attention has been devoted to the insulin-like growth factor signalling pathway that has a major influence on fetal size and contains two components encoded by the oppositely imprinted genes, Igf2 (a growth promoting factor expressed from the paternal allele) and Igf2r (a growth inhibitory factor expressed from the maternal allele). These genes fit the parent-offspring conflict hypothesis for the evolution of genomic imprinting. Accumulated evidence indicates that at least one other fetal growth pathway exists that has also fallen under the influence of imprinting. It is clear that not all components of growth regulatory pathways are encoded by imprinted genes and instead it may be that within a pathway the influence of a single gene by each of the parental genomes may be sufficient for parent-offspring conflict to be enacted. A number of imprinted genes have been found to influence energy homeostasis and some, including Igf2 and Grb10, may coordinate growth with glucose-regulated metabolism. Since perturbation of fetal growth can be correlated with metabolic disorders in adulthood these imprinted genes are considered as candidates for involvement in this phenomenon of fetal programming.
一小部分哺乳动物基因受到基因组印记调控,使得在至少某些表达位点只有一个亲本等位基因是活跃的。印记基因具有多种功能,尤其包括对生长的调控。胰岛素样生长因子信号通路受到了大量关注,该通路对胎儿大小有重大影响,且包含两个由印记相反的基因编码的成分,即Igf2(一种从父本等位基因表达的生长促进因子)和Igf2r(一种从母本等位基因表达的生长抑制因子)。这些基因符合基因组印记进化的亲子冲突假说。积累的证据表明,至少还存在另一条受印记影响的胎儿生长通路。很明显,生长调节通路的所有成分并非都由印记基因编码,相反,在一条通路中,每个亲本基因组中单个基因的影响可能足以引发亲子冲突。已发现许多印记基因会影响能量稳态,其中一些基因,包括Igf2和Grb10,可能会协调生长与葡萄糖调节的代谢。由于胎儿生长的扰动可能与成年后的代谢紊乱相关,这些印记基因被视为参与胎儿编程这一现象的候选基因。