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Background  LIM domain binding protein 1 (LDB1) is a transcriptional co-factor, which interacts with multiple transcription factors and other proteins containing LIM domains. Complete inactivation of  Ldb1  in mice resulted in early embryonic lethality with severe patterning defects during gastrulation. Tissue-specific deletions using a conditional knockout allele revealed additional roles of  Ldb1  in the development of the central nervous system, hematopoietic system, and limbs. The goal of the current study was to determine the importance of  Ldb1  function during craniofacial development in mouse embryos.    Results  We generated tissue-specific  Ldb1  mutants using Wnt1-Cre, which causes deletion of a floxed allele in the neural crest; neural crest-derived cells contribute to most of the mesenchyme of the developing face. All examined  Wnt1-Cre;Ldb1    fl/-    mutants suffered from cleft secondary palate. Therefore, we performed a series of experiments to investigate how  Ldb1  regulated palate development. First, we examined the expression of  Ldb1  during normal development, and found that  Ldb1  was expressed broadly in the palatal mesenchyme during early stages of palate development. Second, we compared the morphology of the developing palate in control and  Ldb1  mutant embryos using sections. We found that the mutant palatal shelves had abnormally blunt appearance, and failed to elevate above the tongue at the posterior domain. An in vitro head culture experiment indicated that the elevation defect was not due to interference by the tongue. Finally, in the  Ldb1  mutant palatal shelves, cell proliferation was abnormal in the anterior, and the expression of  Wnt5a ,  Pax9  and  Osr2 , which regulate palatal shelf elevation, was also altered.    Conclusions  The function of  Ldb1  in the neural crest-derived palatal mesenchyme is essential for normal morphogenesis of the secondary palate.

Neural crest-specific deletion of Ldb1 leads to cleft secondary palate with impaired palatal shelf elevation