van Genderen C, Okamura R M, Fariñas I, Quo R G, Parslow T G, Bruhn L, Grosschedl R
Howard Hughes Medical Institute, University of California, San Francisco 94143-0414.
Genes Dev. 1994 Nov 15;8(22):2691-703. doi: 10.1101/gad.8.22.2691.
Lymphoid enhancer factor 1 (LEF-1) is a sequence-specific DNA-binding protein that is expressed in pre-B and T lymphocytes of adult mice, and in the neural crest, mesencephalon, tooth germs, whisker follicles, and other sites during embryogenesis. We have generated mice carrying a homozygous germ-line mutation in the LEF-1 gene that eliminates its protein expression and causes postnatal lethality. The mutant mice lack teeth, mammary glands, whiskers, and hair but show no obvious defects in lymphoid cell populations at birth. The LEF-1-deficient mice also lack the mesencephalic nucleus of the trigeminal nerve, the only neural crest-derived neuronal populations. Together, the pattern of these defects suggest an essential role for LEF-1 in the formation of several organs and structures that require inductive tissue interactions.
淋巴样增强因子1（LEF-1）是一种序列特异性DNA结合蛋白，在成年小鼠的前B淋巴细胞和T淋巴细胞中表达，在胚胎发育过程中也在神经嵴、中脑、牙胚、触须毛囊和其他部位表达。我们构建了在LEF-1基因中携带纯合种系突变的小鼠，该突变消除了其蛋白表达并导致出生后死亡。突变小鼠没有牙齿、乳腺、触须和毛发，但出生时淋巴细胞群体没有明显缺陷。LEF-1缺陷小鼠也缺乏三叉神经的中脑核，这是唯一源自神经嵴的神经元群体。总之，这些缺陷模式表明LEF-1在需要诱导性组织相互作用的几个器官和结构的形成中起着至关重要的作用。
