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      Pitx1 in vivo Promoter Activity and Mechanisms of Positive Autoregulation

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          During early mouse embryogenesis, Pitx1 (pituitary homeobox 1), a member of the bicoid subgroup of paired homeobox-containing transcription factors, marks the stomodeum, oral ectoderm, pituitary and first branchial arch in the anterior part of the embryo and lateral plate mesoderm only in the posterior half of the embryo. We have now defined Pitx1 promoter fragments that mimic the anterior but not posterior expression of Pitx1 in transgenic mice. In addition, we show positive regulation of this promoter in transfection studies by three members of the Pitx1 family (Pitx1, Pitx1b, Pitx2), as well as by a related factor, Otx1. Pitx1 autoregulation depends on DNA-binding and trans-activation domains of Pitx1 and it may be responsible for establishment and/or maintenance of the Pitx1 expression domain.

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          Most cited references 16

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          Pituitary lineage determination by the Prophet of Pit-1 homeodomain factor defective in Ames dwarfism.

          The gene apparently responsible for a heritable form of murine pituitary-dependent dwarfism (Ames dwarf, df) has been positionally cloned, identifying a novel, tissue-specific, paired-like homeodomain transcription factor, termed Prophet of Pit-1 (Prop-1). The df phenotype results from an apparent failure of initial determination of the Pit-1 lineage required for production of growth hormone, prolactin or thyroid-stimulating hormone, resulting in dysmorphogenesis and failure to activate Pit-1 gene expression. These results imply that a cascade of tissue-specific regulators is responsible for the determination and differentiation of specific cell lineages in pituitary organogenesis.
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            Pitx2 regulates lung asymmetry, cardiac positioning and pituitary and tooth morphogenesis.

             S. Lin,  C Kioussi,  Liu Liu (1999)
            Pitx1 and Pitx2 are highly homologous, bicoid-related transcription factors. Pitx2 was initially identified as the gene responsible for the human Rieger syndrome, an autosomal dominant condition that causes developmental abnormalities. Pitx2 is asymmetrically expressed in the left lateral-plate mesoderm, and mutant mice with laterality defects show altered patterns of Pitx2 expression that correlate with changes in the visceral symmetry (situs). Ectopic expression of Pitx2 in the right lateral-plate mesoderm alters looping of the heart and gut and reverses body rotation in chick and Xenopus embryos. Here we describe the phenotype of Pitx2 gene-deleted mice, characterized by defective body-wall closure, right pulmonary isomerism, altered cardiac position, arrest in turning and, subsequently, a block in the determination and proliferation events of anterior pituitary gland and tooth organogenesis. Thus, Pitx2 is a transcription factor that encodes 'leftness' of the lung.
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              Function of Rieger syndrome gene in left-right asymmetry and craniofacial development.

              Rieger syndrome, an autosomal dominant disorder, includes ocular, craniofacial and umbilical abnormalities. The pitx2 homeobox gene, which is mutated in Rieger syndrome, has been proposed to be the effector molecule interpreting left-right axial information from the early embryonic trunk to each organ. Here we have used gene targeting in mice to generate a loss-of-function allele that would be predicted to result in organ randomization or isomerization. Although pitx2-/- embryos had abnormal cardiac morphogenesis, mutant hearts looped in the normal direction. Pitx2-/- embryos had correctly oriented, but arrested, embryonic rotation and right pulmonary isomerism. They also had defective development of the mandibular and maxillary facial prominences, regression of the stomodeum and arrested tooth development. Fgf8 expression was absent, and Bmp4 expression was expanded in the branchial-arch ectoderm. These data reveal a critical role for pitx2 in left-right asymmetry but indicate that pitx2 may function at an intermediate step in cardiac morphogenesis and embryonic rotation.

                Author and article information

                S. Karger AG
                September 2003
                02 October 2003
                : 78
                : 3
                : 129-137
                Laboratoire de Génétique moléculaire, Institut de recherches cliniques de Montréal (IRCM), Montréal, Qué., Canada
                72794 Neuroendocrinology 2003;78:129–137
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 1, References: 49, Pages: 9
                Transgenic Models in Neuroendocrinology


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