Binary cell fate specification during C. elegans embryogenesis driven by reiterated reciprocal asymmetry of TCF POP-1 and its coactivator β-catenin SYS-1
2007
C. elegans embryos exhibit an invariant lineage comprised
primarily of a stepwise binary diversification of anterior-posterior (A-P)
blastomere identities. This binary cell fate specification requires input from
both the Wnt and MAP kinase signaling pathways. The nuclear level of the TCF
protein POP-1 is lowered in all posterior cells. We show here that theβ
-catenin SYS-1 also exhibits reiterated asymmetry throughout multiple
A-P divisions and that this asymmetry is reciprocal to that of POP-1.
Furthermore, we show that SYS-1 functions as a coactivator for POP-1, and that
the SYS-1-to-POP-1 ratio appears critical for both the anterior and posterior
cell fates. A high ratio drives posterior cell fates, whereas a low ratio
drives anterior cell fates. We show that the SYS-1 and POP-1 asymmetries are
regulated independently, each by a subset of genes in the Wnt/MAP kinase
pathways. We propose that two genetic pathways, one increasing SYS-1 and the
other decreasing POP-1 levels, robustly elevate the SYS-1-to-POP-1 ratio in
the posterior cell, thereby driving A-P differential cell fates.
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