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Vol. 13, No. 12, pp. 1601-1613, June 15, 1999
Department of Molecular and Cellular Biology, Harvard University,
The Biological Laboratories, Cambridge, Massachusetts 02138 USA
Nephrogenesis in the mouse kidney begins at embryonic day 11 and
ends ~10 days postpartum. During this period, new nephrons are
continually being generated from a stem-cell population
the nephrogenic mesenchymein response to signals emanating from the tips
of the branching ureter. Relatively little is known about the mechanism
by which the nephrogenic mesenchyme cell population is maintained at
the tips of the ureter in the presence of signals promoting
tubulogenesis. Previous studies have shown that a loss of Bmp7
function leads to kidney defects that are a likely result of
progressive loss of nephrogenic mesenchyme by apoptosis. The studies
presented here demonstrate that BMP7 signaling can prevent apoptosis in
explants of metanephric mesenchyme. The surviving mesenchyme cell
population, however, is not competent to respond to signals promoting
tubulogenesis. In conjunction with FGF2, BMP7 promotes growth and
maintains competence of the mesenchyme in vitro. In addition, FGF2 and
BMP7 signaling, both independently and in combination, inhibit
tubulogenesis. Interestingly, FGF2 and BMP7 also promote expansion of
the stromal progenitor cell population in whole kidney culture. Because
BMP7 is not produced by stromal progenitor cells, these data suggest a
novel interaction between the nephrogenic mesenchyme and stromal
progenitor cell populations. A model for the regulation of
nephrogenesis by FGF and BMP signaling is presented.
[Key Words: Kidney; fibroblast growth factor; bone morphogenetic protein-7; stromal progenitor cell; apoptosis; competence]
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