Takayama K, Danks D M, Salazar E P, Cleaver J E, Weber C A
Biological and Biotechnology Research Program, Lawrence Livermore National Laboratory, Livermore, California 94551-0808, USA.
Hum Mutat. 1997;9(6):519-25. doi: 10.1002/(SICI)1098-1004(1997)9:6<519::AID-HUMU4>3.0.CO;2-X.
Patient TTD183ME is male and has typical trichothiodystrophy characteristics, including brittle hair, ichthyosis, characteristic face with receding chin and protruding ears, sun sensitivity, and mental and growth retardation. The relative amount of NER carried out by a TTD183ME fibroblast cell strain after ultraviolet (UV) exposure was approximately 65% of normal as determined by a method that converts repair patches into quantifiable DNA breaks. UV survival curves show a reduction in survival only at doses greater than 4 J/m2. Nucleotide sequence analysis of the ERCC2 (XPD) DNA repair and transcription gene cDNA revealed both a Leu461-to-Val substitution and a deletion of amino acids 716-730 in one allele and an Ala725-to-Pro substitution in the other allele. The first allele has also been reported in one xeroderma pigmentosum group D patient and two other trichothiodystrophy patients, while the second allele has not been previously reported. Comparisons suggest that the mutation of Ala725 to Pro correlates with TTD with intermediate UV sensitivity.
患者TTD183ME为男性,具有典型的毛发硫营养不良特征,包括头发脆弱、鱼鳞病、下巴后缩和耳朵突出的特征性面容、对阳光敏感以及智力和生长发育迟缓。通过将修复补丁转化为可量化的DNA断裂的方法测定,紫外线(UV)照射后TTD183ME成纤维细胞株进行的核苷酸切除修复(NER)的相对量约为正常水平的65%。紫外线存活曲线显示,仅在剂量大于4 J/m2时存活率才会降低。ERCC2(XPD)DNA修复和转录基因cDNA的核苷酸序列分析显示,一个等位基因中存在Leu461到Val的替换以及氨基酸716 - 730的缺失,另一个等位基因中存在Ala725到Pro的替换。第一个等位基因也曾在一名着色性干皮病D组患者和另外两名毛发硫营养不良患者中报道过,而第二个等位基因此前尚未见报道。比较表明,Ala725突变为Pro与具有中等紫外线敏感性的毛发硫营养不良相关。