Mucenski M L, McLain K, Kier A B, Swerdlow S H, Schreiner C M, Miller T A, Pietryga D W, Scott W J, Potter S S
Children's Hospital Research Foundation, Department of Pediatrics, Cincinnati, Ohio.
Cell. 1991 May 17;65(4):677-89. doi: 10.1016/0092-8674(91)90099-k.
The c-myb proto-oncogene encodes a sequence-specific DNA-binding protein. To better understand its normal biological function, we have altered the c-myb gene by homologous recombination in mouse embryonic stem cells. Resulting homozygous c-myb mutant mice displayed an interesting phenotype. At day 13 of gestation these mice appeared normal, suggesting that c-myb is not essential for early development. By day 15, however, the mutant mice were severely anemic. Analysis indicated that embryonic erythropoiesis, which occurs in the yolk sac, was not impaired by the c-myb alteration. Adult-type erythropoiesis, which first takes place in the fetal liver, was greatly diminished in c-myb mutants, however. Additional hematopoietic lineages were similarly affected. These results are compatible with a role for c-myb in maintaining the proliferative state of hematopoietic progenitor cells.
c-myb原癌基因编码一种序列特异性DNA结合蛋白。为了更好地理解其正常生物学功能，我们通过同源重组在小鼠胚胎干细胞中改变了c-myb基因。产生的纯合c-myb突变小鼠表现出一种有趣的表型。在妊娠第13天，这些小鼠看起来正常，这表明c-myb对早期发育不是必需的。然而，到第15天，突变小鼠出现严重贫血。分析表明，发生在卵黄囊的胚胎红细胞生成并未受到c-myb改变的影响。然而，首先在胎儿肝脏中发生的成年型红细胞生成在c-myb突变体中大大减少。其他造血谱系也受到类似影响。这些结果与c-myb在维持造血祖细胞增殖状态中的作用相符。
