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Vol. 10, Issue 4, 1221-1234, April 1999
Type II Receptor in Mouse Mammary Stroma Results in
Increased Epithelial Branching
Department of Cell Biology and The Vanderbilt Cancer Center,
Vanderbilt University, Nashville, Tennessee 37232
Members of the transforming growth factor-
(TGF-) superfamily
signal through heteromeric type I and type II serine/threonine kinase
receptors. Transgenic mice that overexpress a dominant-negative mutation of the TGF- type II receptor (DNIIR) under the control of a
metallothionein-derived promoter (MT-DNIIR) were used to determine the
role of endogenous TGF-s in the developing mammary gland. The
expression of the dominant-negative receptor was induced with zinc and
was primarily localized to the stroma underlying the ductal epithelium
in the mammary glands of virgin transgenic mice from two separate mouse
lines. In MT-DNIIR virgin females treated with zinc, there was an
increase in lateral branching of the ductal epithelium. We tested the
hypothesis that expression of the dominant-negative receptor may alter
expression of genes that are expressed in the stroma and regulated by
TGF-s, potentially resulting in the increased lateral branching seen
in the MT-DNIIR mammary glands. The expression of hepatocyte growth
factor mRNA was increased in mammary glands from transgenic animals
relative to the wild-type controls, suggesting that this factor may
play a role in TGF--mediated regulation of lateral branching. Loss of responsiveness to TGF-s in the mammary stroma resulted in increased branching in mammary epithelium, suggesting that TGF-s play an important role in the stromal-epithelial interactions required
for branching morphogenesis.
Corresponding author.
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