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J Biol Chem, Vol. 274, Issue 50, 35331-35336, December 10, 1999
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From The signal transducer and transcriptional
activator STAT5b is required to maintain the adult male pattern of
liver gene expression and whole body pubertal growth rates, as
demonstrated by the loss of these growth hormone (GH)
pulse-dependent responses in mice with a targeted
disruption of the STAT5b gene. The present study investigates whether these phenotypes of STAT5b-deficient mice result
from impaired intracellular GH signaling associated with a loss of GH
pulse responsiveness, as contrasted with a feminization of the
pituitary GH secretory profile leading to the observed feminization of
body growth and liver gene expression. Pulsatile GH replacement in
hypophysectomized mice stimulated body weight gain in wild-type but not
in STAT5b-deficient mice. Expression of the male-specific liver P450
enzyme CYP2D9, which is reduced to female levels in hypophysectomized
male mice, was restored to male levels by GH pulse replacement in
wild-type but not in STAT5b-deficient mice. Similarly, a
female-specific liver CYP2B P450 enzyme that was up-regulated to female
levels following hypophysectomy of males was suppressed to normal basal
male levels by GH pulses only in wild-type hypophysectomized mice.
Finally, urinary excretion of the male-specific, GH pulse-induced major
urinary protein was restored to normal male levels following pulsatile
GH treatment only in the case of wild-type hypophysectomized mice.
STAT5b-deficient mice are thus GH pulse-resistant, supporting the
proposed role of STAT5b as a key intracellular mediator of the
stimulatory effects of plasma GH pulses on the male pattern of liver
gene expression.
AgResearch, Ruakura Research Centre,
Private Bag 3123, Hamilton, New Zealand, the Division of Cell
and Molecular Biology, Department of Biology, Boston University,
Boston, Massachusetts 02215, and the ** Department of Anatomy and
Structural Biology, School of Medical Sciences, University of Otago,
Dunedin, New Zealand
To whom correspondence may be addressed. Fax: 617-353-7404;
E-mail: djw@bio.bu.edu.
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