Journal
DEVELOPMENTAL DYNAMICS
Volume 237, Issue 4, Pages 1006-1020Publisher
WILEY-LISS
DOI: 10.1002/dvdy.21511
Keywords
Wnt5a; Wnt4; Wnt6; Wnt11; Wnt16; mouse knockout; development
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Funding
- NICHD NIH HHS [R37 HD030428, R37 HD030428-17, R01 HD034283-13, R01-HD34283, R37-HD30428, R01 HD034283] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007863, GM07863] Funding Source: Medline
- FDA HHS [2-T32-BM0832213] Funding Source: Medline
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We examined the role of WNT signaling in pituitary development by characterizing the pituitary phenotype of three WNT knockout mice and assessing the expression of WNT pathway components. Wnt5a mutants have expanded domains of Fgf10 and bone morphogenetic protein expression in the ventral diencephalon and a reduced domain of LHX3 expression in Rathke's pouch. Wnt4 mutants have mildly reduced cell differentiation, reduced POU1F1 expression, and mild anterior lobe hypoplasia. Wnt4, Wnt5a double mutants exhibit an additive pituitary phenotype of dysmorphology and mild hypoplasia. Wnt6 mutants have no obvious pituitary phenotype. We surveyed WNT expression and identified transcripts for numerous Wnts, Frizzleds, and downstream pathway members in the pituitary and ventral diencephalon. These findings support the emerging model that WNT signaling affects the pituitary gland via effects on ventral diencephalon signaling, and suggest additional Wnt genes that are worthy of functional studies.
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