Complex functional redundancy of Tbx2 and Tbx3 in mouse limb development

被引:2
|
作者
Lopatka, Alika [1 ]
Moon, Anne M. [1 ,2 ,3 ]
机构
[1] Geisinger Med Clin, Dept Mol & Funct Genom, Weis Ctr Res, Danville, PA USA
[2] Univ Utah, Dept Human Genet, Salt Lake City, UT 84112 USA
[3] Hess Ctr Sci & Med Mt Sinai, Mindich Child Hlth & Dev Inst, New York, NY USA
关键词
limb development; T-box; Tbx2; Tbx3; ulnar-mammary syndrome; T-BOX GENES; ULNAR-MAMMARY SYNDROME; OUTFLOW TRACT; IDENTITY; MICE; MORPHOGENESIS; MUTATIONS; DEFECTS; PROTEIN; ROLES;
D O I
10.1002/dvdy.484
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
The limb phenotypes of Tbx2 and Tbx3 mutants are distinct: loss of Tbx2 results in isolated duplication of digit 4 in the hindlimb while loss of Tbx3 results in anterior polydactyly and posterior oligodactly in the forelimb. In the face of such disparate phenotypes, we sought to determine whether Tbx2 and Tbx3 have functional redundancy during development of the mouse limb. We found that sequential loss of alleles generates defects that are not simply additive of those observed in single mutants and that multiple structures in both the forelimb and hindlimb display compound sensitivity to decreased gene dosage.
引用
收藏
页码:1613 / 1627
页数:15
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