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Immunodeficiency: when T cells are stuck at home

机译：免疫缺陷：当T细胞卡在家里时

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The cataract Shionogi (CTS) strain of mouse was initially described in 1968 as having cataracts and micropthalmia and was later reported to have profound peripheral T cell deficiency (Ptcd). The nature of this defect, however, has remained unclear. In this issue of Nature Immunology, Cyster and colleagues map the genetic basis of the T cell deficiency in CTS mice and show that it is caused by a point mutation in Corola, the gene encoding the actin-regulating protein coronin 1A (CorolA). By mapping a cross between CTS and C57BL/6 mice, they find that cataracts and microphthalmia fail to segregate with Ptcd. They further map the Ptcd locus to a 950-kilobase interval of DNA on chromosome 7, which contains 37 open reading frames, including Corola. By sequencing, they identify a G-to-A mutation in exon 2 of Corola that results in the substitution of lysine for a highly conserved glutamic acid residue at position 26. They confirm that this E26K substitution causes Ptcd by complementation with Corola~(+/-) mice, in which the wild-type allele complements the phenotype but the null allele does not
机译：最初在1968年将小鼠的白内障Shionogi（CTS）菌株描述为患有白内障和微眼睑炎，后来报道其患有严重的外周T细胞缺乏症（Ptcd）。但是，这种缺陷的性质仍不清楚。在本期《自然免疫学》中，Cyster及其同事绘制了CTS小鼠T细胞缺乏症的遗传基础，并表明这是由Corola中的点突变引起的，Corola是编码肌动蛋白调节蛋白coronin 1A（CorolA）的基因。通过绘制CTS和C57BL / 6小鼠之间的杂交图，他们发现白内障和小眼症无法与Ptcd隔离。他们进一步将Ptcd基因座映射到7号染色体上950碱基对的DNA间隔，该DNA包含37个开放阅读框，包括Corola。通过测序，他们确定了Corola外显子2中的G-to-A突变，该突变导致赖氨酸被26位的高度保守的谷氨酸残基取代。他们证实，这种E26K取代通过与Corola〜（+ /-）小鼠，其中野生型等位基因与表型互补，而无效等位基因则不

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