Quane K A, Keating K E, Healy J M, Manning B M, Krivosic-Horber R, Krivosic I, Monnier N, Lunardi J, McCarthy T V
Department of Biochemistry, University College, Cork, Ireland.
Genomics. 1994 Sep 1;23(1):236-9. doi: 10.1006/geno.1994.1483.
The ryanodine receptor gene (RYR1) has been shown to be mutated in a small number of malignant hyperthermia (MH) pedigrees. Missense mutations in this gene have also been identified in two families with central core disease (CCD), a rare myopathy closely associated with MH. In an effort to identify other RYR1 mutations responsible for MH and CCD, we used a SSCP approach to screen the RYR1 gene for mutations in a family exhibiting susceptibility to MH (MHS) where some of the MHS individuals display core regions in their muscle. Sequence analysis of a unique aberrant SSCP has allowed us to identify a point mutation cosegregating with MHS in the described family. The mutation changes a conserved tyrosine residue at position 522 to a serine residue. This mutation is positioned relatively close to five of the six MHS/CCD mutations known to date and provides further evidence that MHS/CCD mutations may cluster in the amino terminal region of the RYR1 protein.
已证实,在少数恶性高热(MH)家系中,雷诺丁受体基因(RYR1)发生了突变。在两个患有中央轴空病(CCD)的家族中也发现了该基因的错义突变,CCD是一种与MH密切相关的罕见肌病。为了确定导致MH和CCD的其他RYR1突变,我们采用单链构象多态性(SSCP)方法,对一个表现出MH易感性(MHS)的家族中的RYR1基因进行突变筛查,该家族中的一些MHS个体肌肉中存在核心区域。对一个独特的异常SSCP进行序列分析,使我们能够在所述家族中鉴定出一个与MHS共分离的点突变。该突变将第522位保守的酪氨酸残基改变为丝氨酸残基。此突变的位置相对靠近迄今已知的六个MHS/CCD突变中的五个,这进一步证明MHS/CCD突变可能聚集在RYR1蛋白的氨基末端区域。