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Figure 6


Fig. 6. Signal transduction through the MEK/ERK pathway is defective in svs mutant mice. (A) Western blots of P5 seminal vesicles from svs mutant and heterozygous control mice showing the loss of activated ERK1/2 in seminal vesicles from the svs mutant mice. (B) Western blot of seminal vesicles from P1 wild-type mice stimulated with recombinant FGF10 protein for 0, 20, 40 or 120 minutes, revealing a 2-fold activation of ERK1/2 by 20 minutes of stimulation, which recedes to near basal levels by 2 hours. Graph below shows quantification of the western blot results. (C) P1 wild-type seminal vesicles were cultured in serum-free medium (data not shown), serum-free medium plus testosterone (T), or serum-free medium with testosterone and UO126 (T+UO126). Testosterone stimulates lateral branching during a 4-day culture period (arrowhead). UO126 completely abrogates all testosterone-induced branching (bottom panels). (D) Western blot of cultured seminal vesicles confirms that testosterone does not stimulate activation of ERK1/2, and that UO126 inhibits ERK1/2 phosphorylation.





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