Complex functional redundancy of Tbx2 and Tbx3 in mouse limb development.

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. Key Findings: Loss of Tbx2 and Tbx3 in early mouse limb causes defects that are more than additive of those seen in single mutants.Novel phenotypes occur with loss of both factors.Redundancy has been hypothesized, here it is tested. [ABSTRACT FROM AUTHOR]