Delaval Katia, Wagschal Alexandre, Feil Robert
Institute of Molecular Genetics, CNRS, UMR-5535, University of Montpellier II, France.
Bioessays. 2006 May;28(5):453-9. doi: 10.1002/bies.20407.
Human chromosome 11p15 comprises two imprinted domains important in the control of fetal and postnatal growth. Novel studies establish that imprinting at one of these, the IGF2-H19 domain, is epigenetically deregulated (with loss of DNA methylation) in Silver-Russell Syndrome (SRS), a congenital disease of growth retardation and asymmetry. Previously, the exact opposite epigenetic alteration (gain of DNA methylation) had been detected at the domain's 'imprinting control region' (ICR) in patients with Beckwith-Wiedemann Syndrome (BWS), a complex disorder of fetal overgrowth. However, more frequently, BWS is caused by loss of DNA methylation at the ICR that regulates the second imprinted domain at 11p15. Interestingly, a similar epigenetic alteration (with loss of methylation) at a putative ICR on human chromosome 6q24, is involved in transient neonatal diabetes mellitus (TNDM), a congenital disease with intrauterine growth retardation and a transient lack of insulin. Thus, fetal and postnatal growth is epigenetically controlled by different ICRs, at 11p15 and other chromosomal regions.
人类染色体11p15包含两个在胎儿和出生后生长控制中起重要作用的印记区域。新的研究表明,在Silver-Russell综合征(SRS)中,其中一个区域(IGF2-H19区域)的印记在表观遗传上失调(DNA甲基化缺失),SRS是一种先天性生长发育迟缓与不对称的疾病。此前,在Beckwith-Wiedemann综合征(BWS)患者的该区域“印记控制区”(ICR)检测到完全相反的表观遗传改变(DNA甲基化增加),BWS是一种胎儿过度生长的复杂疾病。然而,更常见的是,BWS是由调控11p15第二个印记区域的ICR处DNA甲基化缺失引起的。有趣的是,人类染色体6q24上一个假定的ICR处类似的表观遗传改变(甲基化缺失)与短暂性新生儿糖尿病(TNDM)有关,TNDM是一种伴有宫内生长迟缓及短暂胰岛素缺乏的先天性疾病。因此,胎儿和出生后的生长在表观遗传上由11p15和其他染色体区域的不同ICR控制。