GATA6 regulates HNF4 and is required for differentiation of visceral endoderm in the mouse embryo

Article Abstract:

GATA6 regulates HNF4. It is required for differentiation of visceral endoderm in the mouse embryo. Its function in embryonic development has been investigated through use of gene targeting to generate mice with a null mutation in GATA6 and GATA6-deficient ES cells and GATA6-deficient ES cells. Homozygous GATA6-/- mice died between the 6.5th and the 7.5th embryonic days and showed a specific defect in endoderm differentiation. The defect included absence of HNF4 gene expression and severely down-regulated expression of GATA4. Data indicate a model in which GATA6 is upstream from HNF4 in a transcription cascade that regulates differentiation of the visceral endoderm. It appears that GATA6 is necessary for establishing the endodermally derived bronchial epithelium.

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Cytosine methylation and mammalian development

Article Abstract:

Programmed methylation and demethylation of regulatory sequences has been proposed to play a central role, in vertebrate development. The methylation status of 5' regions of a panel of tissue-specific genes has not been correlated with expression in tissues of fetal and newborn mice despite efforts to do so. A model in which cytosine methylation is a biochemical specialization of large genomes and participates in specialized biological functions, among them allele-specific gene expression and heritable transcriptional silencing of parasitic sequence elements. Cellular differentiation is regulated by conserved regulatory networks. These networks do not depend on covalent modification of the genome.

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Caenorhabditis elegans Akt/PKB transduces insulin receptor-like signals from AGE-1 PI3 kinase to the DAF-16 transcription factor

Article Abstract:

A neurosecretory pathway controls a reversible developmental arrest and metabolic shift in the dauer larval stage of Caenorhabditis elegans. Defects in a signaling pathway like that of insulin cause arrest. Akt/PKB transduces signals like those of an insulin receptor to the DAF-16 transcription factor from AGE-1 PI3 kinase.

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