ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2009
The Pitx2c N-terminal domain is a critical interaction domain required for asymmetric morphogenesis.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Teaching an old dog new tricks: reactivated developmental signaling pathways regulate ABCB1 and chemoresistance in cancer.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- PITX2 Loss-of-Function Mutation Contributes to Congenital Endocardial Cushion Defect and Axenfeld-Rieger Syndrome.PloS one · 2015Article
- Prevalence and spectrum of PITX2c mutations associated with congenital heart disease.DNA and cell biology · 2013Article
- Pleiotropic and isoform-specific functions for Pitx2 in superior colliculus and hypothalamic neuronal development.Molecular and cellular neurosciences · 2013Article
- PITX2c loss-of-function mutations responsible for congenital atrial septal defects.International journal of medical sciences · 2013Article
- A zebrafish model of axenfeld-rieger syndrome reveals that pitx2 regulation by retinoic acid is essential for ocular and craniofacial development.Investigative ophthalmology & visual science · 2012Article
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Authors and funding
6 authors.
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Abstract
The paired-like homeodomain transcription factor Pitx2c has an essential role in patterning the left-right axis. However, neither its transcriptional targets nor the molecular mechanisms through which it exerts its patterning function are known. Here we provide evidence that the N-terminal domain of Pitx2c is important for this activity. Overexpression of the Pitx2c N-terminus in ovo randomizes the direction of heart looping, the first morphological asymmetry conserved in vertebrate embryos. In addition, the Pitx2c N-terminal domain blocks the ability of Pitx2c to synergize with Nkx2.5 to transactivate the procollagen lysyl hydroxylase (Plod-1) promoter in transient transfection assays. A five amino acid region containing leucine-41 is required for both of these effects. Our data suggest that the Pitx2c N-terminal domain competes with endogenous Pitx2c for binding to a protein interaction partner that is required for the activation of genes that direct asymmetric morphogenesis along the left-right axis.
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