Targeted inactivation of Hoxb8 affects survival of a spinal ganglion and causes aberrant limb reflexes

被引：58

作者：

van den Akker, E ^{[1
]}

Reijnen, M ^{[1
]}

Korving, J ^{[1
]}

Brouwer, A ^{[1
]}

Meijlink, F ^{[1
]}

Deschamps, J ^{[1
]}

机构：

[1] Netherlands Inst Dev Biol, Hubrecht Lab, NL-3584 CT Utrecht, Netherlands

来源：

MECHANISMS OF DEVELOPMENT | 1999年 / 89卷 / 1-2期

关键词：

Hoxb8; patterning; spinal ganglia; vertebra; limb;

D O I：

10.1016/S0925-4773(99)00212-9

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Hoxb8 mutant mice were generated by inserting the lacZ coding sequence in Frame with the first exon of Hoxb8. These mice express a fusion protein with a functional P-galactosidase activity instead of Hoxb8, Mutant embryos were analyzed for anatomical changes. The results indicate that Hoxb8 is not an indispensable regulator of A-P patterning in the forelimb, unlike suggested by our Hoxb8 gain of function experiments (Charite J, DeGraaff W, Shen S, Deschamps J. Cell 1994;78:589-601). The null mutant phenotypic traits include degeneration of the second spinal ganglion (C2), an abnormality opposite to the alteration in the gain of function transgenic mice. Subtle changes in the thoracic part of the vertebral column were observed as well. Adult homozygous mutants exhibit an abnormal clasping reflex of the limbs. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：103 / 114

页数：12