首页 | 本学科首页   官方微博 | 高级检索  
   检索      


Clinical expression of Leber hereditary optic neuropathy is affected by the mitochondrial DNA-haplogroup background
Authors:Hudson Gavin  Carelli Valerio  Spruijt Liesbeth  Gerards Mike  Mowbray Catherine  Achilli Alessandro  Pyle Angela  Elson Joanna  Howell Neil  La Morgia Chiara  Valentino Maria Lucia  Huoponen Kirsi  Savontaus Marja-Liisa  Nikoskelainen Eeva  Sadun Alfredo A  Salomao Solange R  Belfort Rubens  Griffiths Philip  Man Patrick Yu Wai  de Coo Rene F M  Horvath Rita  Zeviani Massimo  Smeets Hubert J T  Torroni Antonio  Chinnery Patrick F
Institution:Mitochondrial Research Group, Department of Ophthalmology and Institute of Human Genetics, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK.
Abstract:Leber hereditary optic neuropathy (LHON) is due primarily to one of three common point mutations of mitochondrial DNA (mtDNA), but the incomplete penetrance implicates additional genetic or environmental factors in the pathophysiology of the disorder. Both the 11778G-->A and 14484T-->C LHON mutations are preferentially found on a specific mtDNA genetic background, but 3460G-->A is not. However, there is no clear evidence that any background influences clinical penetrance in any of these mutations. By studying 3,613 subjects from 159 LHON-affected pedigrees, we show that the risk of visual failure is greater when the 11778G-->A or 14484T-->C mutations are present in specific subgroups of haplogroup J (J2 for 11778G-->A and J1 for 14484T-->C) and when the 3460G-->A mutation is present in haplogroup K. By contrast, the risk of visual failure is significantly less when 11778G-->A occurs in haplogroup H. Substitutions on MTCYB provide an explanation for these findings, which demonstrate that common genetic variants have a marked effect on the expression of an ostensibly monogenic mtDNA disorder.
Keywords:
本文献已被 ScienceDirect PubMed 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号