Tsakiri Kalliopi D, Cronkhite Jennifer T, Kuan Phillip J, Xing Chao, Raghu Ganesh, Weissler Jonathan C, Rosenblatt Randall L, Shay Jerry W, Garcia Christine Kim
McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
Proc Natl Acad Sci U S A. 2007 May 1;104(18):7552-7. doi: 10.1073/pnas.0701009104. Epub 2007 Apr 25.
Idiopathic pulmonary fibrosis (IPF) is an adult-onset, lethal, scarring lung disease of unknown etiology. Some individuals with IPF have a familial disorder that segregates as a dominant trait with incomplete penetrance. Here we used linkage to map the disease gene in two families to chromosome 5. Sequencing a candidate gene within the interval, TERT, revealed a missense mutation and a frameshift mutation that cosegregated with pulmonary disease in the two families. TERT encodes telomerase reverse transcriptase, which together with the RNA component of telomerase (TERC), is required to maintain telomere integrity. Sequencing the probands of 44 additional unrelated families and 44 sporadic cases of interstitial lung disease revealed five other mutations in TERT. A heterozygous mutation in TERC also was found in one family. Heterozygous carriers of all of the mutations in TERT or TERC had shorter telomeres than age-matched family members without the mutations. Thus, mutations in TERT or TERC that result in telomere shortening over time confer a dramatic increase in susceptibility to adult-onset IPF.
特发性肺纤维化(IPF)是一种成年起病、致命的、病因不明的瘢痕性肺病。一些特发性肺纤维化患者患有家族性疾病,该疾病作为一种显性性状分离,且具有不完全外显率。在此,我们通过连锁分析将两个家族中的疾病基因定位到5号染色体。对该区间内的一个候选基因TERT进行测序,发现了一个错义突变和一个移码突变,这两个突变在两个家族中均与肺部疾病共分离。TERT编码端粒酶逆转录酶,它与端粒酶的RNA成分(TERC)共同作用,维持端粒完整性。对另外44个不相关家族的先证者以及44例散发性间质性肺病病例进行测序,发现TERT还有其他五个突变。在一个家族中还发现了TERC的一个杂合突变。TERT或TERC中所有突变的杂合携带者的端粒比没有这些突变的年龄匹配家族成员的端粒短。因此,随着时间推移导致端粒缩短的TERT或TERC突变会显著增加成年起病的特发性肺纤维化的易感性。