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Fig. 8. A model for specification of the MS blastomere. A gene cascade that
begins with maternal SKN-1 progresses through activation of med-1,2
in EMS, which in turn activate tbx-35 in MS. POP-1 represses endoderm
specification in MS. In E, the sister of MS, a Wnt/MAPK-dependent mechanism
represses tbx-35 through an unknown effector (not shown). TBX-35 acts
upstream of genes that specify pharynx and muscle fates, through regulators
such as pha-4 and hlh-1, respectively
(Gaudet and Mango, 2002;
Krause et al., 1990). TBX-35
also represses targets of maternal PAL-1, blocking C fates. Activation of
med-1,2 by SKN-1 is direct
(Maduro et al., 2001), as is
activation of tbx-35 by MED-1,2 (this work). In addition to
med-1,2, SKN-1 also activates the expression of one or more
Delta/Serrate/Lag (DSL) proteins that enable the MS cell to signal the AB
lineage to make anterior pharynx (Priess
et al., 1987).
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