Tbx10, a member of the T-box gene family, is associated with multiple biological processes. T-box genes encode transcription factors that play crucial roles in the development of several tissues, controlling basic processes like cell differentiation [4,5]. The human TBX10 gene is mapped to chromosome 11q13, a region linked to multiple inherited developmental disorders, suggesting its potential importance in development and disease [2]. Genetic models, such as mouse models, are valuable for studying its function.

To study Tbx10, Tbx10(LacZ/+) mice were created by replacing the T-box coding region with a LacZ gene. X-gal staining showed LacZ(+) cells in rhombomere 4 and rhombomere 6 of the hindbrain, present in both embryonic and adult mice. These cells in rhombomere 4 are a subpopulation of ventral interneurons in the pons, indicating its role in hindbrain development [1]. In Dancer mutant mice, an insertion in the first intron of Tbx10 causes ectopic expression of a p23-Tbx10 chimeric transcript. Ectopic expression of Tbx10 in transgenic mice recapitulates the Dancer mutant phenotype of cleft lip and palate, showing that gain-of-function of Tbx10 can lead to this birth defect [3].

In conclusion, Tbx10 is important for hindbrain development, as seen from the LacZ-marked cell populations in mouse models. Its abnormal gain-of-function can result in cleft lip and palate defects in mice. These model-based studies help in understanding the role of Tbx10 in normal development and the pathogenesis of certain birth defects [1,3].