Journal
MOLECULAR ENDOCRINOLOGY
Volume 20, Issue 6, Pages 1366-1377Publisher
OXFORD UNIV PRESS INC
DOI: 10.1210/me.2005-0378
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Funding
- NCI NIH HHS [R01 CA47411, CA46592] Funding Source: Medline
- NIAMS NIH HHS [AR20557] Funding Source: Medline
- NICHD NIH HHS [R01 HD34283, U54-HD28934] Funding Source: Medline
- NIDDK NIH HHS [R01 DK36843, DK07367] Funding Source: Medline
- NIGMS NIH HHS [T32 GM07863] Funding Source: Medline
- FDA HHS [56-T32-BM07544] Funding Source: Medline
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GATA2 is expressed in the pituitary during development and in adult gonadotropes and thyrotropes. It is proposed to be important for gonadotrope and thyrotrope cell fate choice and for TSH production. To test this idea, we produced a pituitary-specific knockout of Gata2, designed so that the DNA-binding zinc-finger region is deleted in the presence of a pituitary-specific recombinase transgene. These mice have reduced secretion of gonadotropins basally and in response to castration challenge, although the mice are fertile. GATA2 deficiency also compromises thyrotrope function. Mutants have fewer thyrotrope cells at birth, male Gata2-deficient mice exhibit growth delay from 3 - 9 wk of age, and adult mutants produce less TSH in response to severe hypothyroidism after radiothyroidectomy. Therefore, Gata2 appears to be dispensable for gonadotrope and thyrotrope cell fate and maintenance, but important for optimal gonadotrope and thyrotrope function. Gata2-deficient mice exhibit elevated levels of Gata3 transcripts in the pituitary gland, suggesting that GATA3 can compensate for GATA2.
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