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与科芬-洛里综合征相关的激酶Rsk-2中的突变。

Mutations in the kinase Rsk-2 associated with Coffin-Lowry syndrome.

作者信息

Trivier E, De Cesare D, Jacquot S, Pannetier S, Zackai E, Young I, Mandel J L, Sassone-Corsi P, Hanauer A

机构信息

Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS,INSERM, Illkirch, France.

出版信息

Nature. 1996 Dec 12;384(6609):567-70. doi: 10.1038/384567a0.

Abstract

The Coffin-Lowry syndrome (CLS), an X-linked disorder, is characterized by severe psychomotor retardation, facial and digital dysmorphisms, and progressive skeletal deformations. Genetic linkage analysis mapped the CLS locus to an interval of 2-3 megabases at Xp22.2. The gene coding for Rsk-2, a member of the growth-factor-regulated protein kinases, maps within the candidate interval, and was tested as a candidate gene for CLS. Initial screening for mutations in the gene for Rsk-2 in 76 unrelated CLS patients revealed one intragenic deletion, a nonsense, two splice site, and two missense mutations. The two missenses affect sites critical for the function of Rsk-2. The mutated Rsk-2 proteins were found to be inactive in a S6 kinase assay. These findings provide direct evidence that abnormalities in the MAPK/RSK signalling pathway cause Coffin-Lowry syndrome.

摘要

科芬-洛里综合征(CLS)是一种X连锁疾病,其特征为严重的精神运动发育迟缓、面部和手部畸形以及进行性骨骼变形。基因连锁分析将CLS基因座定位到Xp22.2上2-3兆碱基的区间。编码Rsk-2(一种生长因子调节蛋白激酶家族成员)的基因位于该候选区间内,并被作为CLS的候选基因进行检测。对76名无亲缘关系的CLS患者的Rsk-2基因进行突变初步筛查,发现了1个基因内缺失、1个无义突变、2个剪接位点突变和2个错义突变。这两个错义突变影响Rsk-2功能的关键位点。在S6激酶检测中发现突变的Rsk-2蛋白无活性。这些发现提供了直接证据,表明MAPK/RSK信号通路异常导致科芬-洛里综合征。

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