The Mediator complex can transmit activities of various transcription factors to RNA ploymerase to regulate transcription in vitro . However, its function in animal development is unclear. We have identified mutants in
dpy-22 and
let-19 by their defects in asymmetric cell divisions regulated by
lin-44/wnt and
lin-17/frizzled . We found that these genes encode homologs of TRAP230 and TRAP240 that are components of the Mediator complex. Weak mutations of
dpy-22 /TRAP230 were reported previously as
sop-1 mutations that suppress
pal-1 mutants but do not have appparent phenotypes by themselves (1).
dpy-22 and
let-19 mutants also show defects in cell fusion regulated by
bar-1 /beta-catenin, indicating that these genes functions in the Wnt signaling pathway. In addition to their defects in Wnt signaling,
dpy-22 and
let-19 mutants also show multivulva (Muv) phenotype. The induction of vulva is regulated by
lin-12/notch and
let-60/ras . Ras signaling promotes a cell fate called primary while Notch signaling induces the secondary cell fate. In
let-19 mutants, secondary lineages are ectopically induced, suggesting that
let-19 functions in
lin-12/notch pathway. In contrast, another components of Mediator, SUR-2 and LET-425/MED6, was shown to function downstream of
let-60/ras (2, 3). Furthermore, we found that
let-425 but not
sur-2 can suppress gain-of-function mutations in
lin-12 as well as
let-60(gf) . These results indicate that both Ras and Notch signals are transmitted to Mediator to regulate three cell fates during vulval induction. We will discuss functions of Mediator in the integration of the signaling pathways. (1) Zhang, H., and Emmons, S. W. (2000) Genes Dev 14, 2161-72. (2) Singh, N., and Han, M. (1995) Genes Dev 9, 2251-2265. (3) Kwon, J. Y., and Lee, J. (2001) Development 128, 3095-3104.