Kobayashi K, Jackson M J, Tick D B, O'Brien W E, Beaudet A L
Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030.
J Biol Chem. 1990 Jul 5;265(19):11361-7.
Citrullinemia is an autosomal recessive disease caused by deficiency of argininosuccinate synthetase. In order to characterize mutations, RNA was isolated from cultured fibroblasts from 13 unrelated patients with neonatal citrullinemia. Ten mutations were identified by sequencing of amplified cDNA. Seven single base missense mutations were identified: Gly14----Ser, Ser180----Asn, Arg157----His, Arg304----Trp, Gly324----Ser, Arg363----Trp, and Gly390----Arg. Six of these missense mutations involved conversion of a CpG dinucleotide in the sense strand to TpG or CpA, and six of the seven mutations alter a restriction enzyme site in the cDNA. Two mutations were observed in which the sequences encoded by a single exon (exon 7 or 13) were absent from the cDNA. One mutation is a G----C substitution in the last position of intron 15 resulting in splicing to a cryptic splice site within exon 16. There is extreme heterogeneity of mutations causing citrulinemia. This heterogeneity may prove typical for less common autosomal recessive human genetic diseases.
瓜氨酸血症是一种由精氨琥珀酸合成酶缺乏引起的常染色体隐性疾病。为了鉴定突变,从13名无关的新生儿瓜氨酸血症患者培养的成纤维细胞中分离出RNA。通过对扩增的cDNA进行测序鉴定出10种突变。鉴定出7种单碱基错义突变:Gly14→Ser、Ser180→Asn、Arg157→His、Arg304→Trp、Gly324→Ser、Arg363→Trp和Gly390→Arg。这些错义突变中的6种涉及有义链中一个CpG二核苷酸转换为TpG或CpA,并且7种突变中的6种改变了cDNA中的一个限制性酶切位点。观察到两种突变,其中cDNA中缺失了由单个外显子(外显子7或13)编码的序列。一种突变是内含子15最后位置的G→C替换,导致剪接到外显子16内的一个隐蔽剪接位点。导致瓜氨酸血症的突变存在极大的异质性。这种异质性可能是较罕见的常染色体隐性人类遗传疾病的典型特征。