Houzelstein D, Cohen A, Buckingham M E, Robert B
CNRS URA 1947, Département de Biologie Moléculaire, Institut Pasteur,Paris, France.
Mech Dev. 1997 Jul;65(1-2):123-33. doi: 10.1016/s0925-4773(97)00065-8.
We have generated a null allele of the mouse Msx1 homeobox gene by insertion of an nlacZ reporter gene into its homeobox. The sensitivity of beta-galactosidase detection permitted us to reveal novel aspects of Msx1 gene expression in heterozygous embryos, in particular in ectoderm and mesoderm during gastrulation, and in migrating neural crest cells. Homozygous mutant mice die at birth with facial defects (see Satokata, I. and Maas, R. (1994) Msx1 deficient mice exhibit cleft palate and abnormalities of craniofacial and tooth development. Nat. Genet. 6, 348-356). To investigate the reason for this limited phenotype, we compared the pattern of Msx1 expression with that of the closely related Msx2 gene in wild type embryos and in Msx1-/- mutants. Notably, whereas the expression of Msx1 and Msx2 overlap in the developing limb, this is not the case in the facial regions most affected in the mutant.
我们通过将一个nlacZ报告基因插入小鼠Msx1同源框基因中，产生了该基因的无效等位基因。β-半乳糖苷酶检测的敏感性使我们能够揭示杂合胚胎中Msx1基因表达的新情况，特别是在原肠胚形成期间在外胚层和中胚层，以及在迁移的神经嵴细胞中的表达。纯合突变小鼠出生时因面部缺陷而死亡（见佐藤伊织和马斯R.（1994年）Msx1基因缺陷小鼠表现出腭裂以及颅面和牙齿发育异常。《自然遗传学》6卷，348 - 356页）。为了研究这种有限表型的原因，我们在野生型胚胎和Msx1 - / - 突变体中比较了Msx1与密切相关的Msx2基因的表达模式。值得注意的是，虽然Msx1和Msx2在发育中的肢体中的表达重叠，但在突变体中受影响最严重的面部区域并非如此。
