Abstract
Hox transcription factors control morphogenesis along the head-tail axis of bilaterians. Because their direct functional targets are still poorly understood in vertebrates, it remains unclear how the positional information encoded by Hox genes is translated into morphogenetic changes. Here, we conclusively demonstrate that Six2 is a direct downstream target of Hoxa2 in vivo and show that the ectopic expression of Six2, observed in the absence of Hoxa2, contributes to the Hoxa2 mouse mutant phenotype. We propose that Six2 acts to mediate Hoxa2 control over the insulin-like growth factor pathway during branchial arch development.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Base Sequence
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Binding Sites / genetics
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Body Patterning
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Branchial Region / embryology
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Branchial Region / metabolism
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DNA Primers / genetics
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Female
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Gene Expression Regulation, Developmental
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Homeodomain Proteins / genetics
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Homeodomain Proteins / metabolism
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Homeodomain Proteins / physiology*
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Homeostasis
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Insulin-Like Growth Factor Binding Protein 5 / genetics
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Mice
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Mice, Knockout
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Mice, Mutant Strains
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Mice, Transgenic
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Phenotype
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Pre-B-Cell Leukemia Transcription Factor 1
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Pregnancy
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Promoter Regions, Genetic
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Signal Transduction
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Somatomedins / metabolism
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Transcription Factors / deficiency
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Transcription Factors / genetics
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Transcription Factors / metabolism
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Transcription Factors / physiology*
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Transcription, Genetic
Substances
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DNA Primers
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Homeodomain Proteins
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Hoxa2 protein, mouse
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Insulin-Like Growth Factor Binding Protein 5
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Pbx1 protein, mouse
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Pre-B-Cell Leukemia Transcription Factor 1
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Six2 protein, mouse
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Somatomedins
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Transcription Factors