Kuroda M, Sok J, Webb L, Baechtold H, Urano F, Yin Y, Chung P, de Rooij D G, Akhmedov A, Ashley T, Ron D
Skirball Institute of Biomolecular Medicine, the Departments of Medicine, Cell Biology and the Kaplan Cancer Center, NYU Medical Center, New York, NY 10016, USA.
EMBO J. 2000 Feb 1;19(3):453-62. doi: 10.1093/emboj/19.3.453.
TLS (also known as FUS) is an RNA-binding protein that contributes the N-terminal half of fusion oncoproteins implicated in the development of human liposarcomas and leukemias. Here we report that male mice homozygous for an induced mutation in TLS are sterile with a marked increase in the number of unpaired and mispaired chromosomal axes in pre-meiotic spermatocytes. Nuclear extracts from TLS(-/-) testes lack an activity capable of promoting pairing between homologous DNA sequences in vitro, and TLS(-/-) mice and embryonic fibroblasts exhibit increased sensitivity to ionizing irradiation. These results are consistent with a role for TLS in homologous DNA pairing and recombination.
TLS（也称为FUS）是一种RNA结合蛋白，它构成了与人类脂肪肉瘤和白血病发生相关的融合癌蛋白的N端一半。我们在此报告，TLS基因发生诱导突变的纯合雄性小鼠不育，减数分裂前精母细胞中未配对和错配的染色体轴数量显著增加。TLS基因敲除小鼠睾丸的核提取物缺乏在体外促进同源DNA序列配对的活性，并且TLS基因敲除小鼠和胚胎成纤维细胞对电离辐射的敏感性增加。这些结果与TLS在同源DNA配对和重组中的作用一致。
