During vulval development, the Ras-mediated inductive signal induces P6.p to adopt the 1<
sym05> fate, while LIN-12/Notch-mediated lateral signaling causes P5.p and P7.p to adopt the 2<
sym05> fate. We have shown that three dsl genes,
lag-2,
apx-1, and
dsl-1, are functionally redundant components of the lateral signal. Transcription of all three genes is initiated or upregulated in VPCs in response to the inductive signal (Chen and Greenwald, 2004).We performed a computational analysis of the 5<
sym07> flanking regions of all three lateral signal genes and identified an <
sym08>EBSX<
sym09> motif, which is composed of Ets Binding Site (EBS) and a conserved flanking sequence (X). We have found that an 800 bp fragment from the
apx-1 promoter that has a cluster of <
sym08>EBSX<
sym09> motifs appears to be necessary and sufficient for expression in the presumptive 1<
sym05> VPC. Furthermore, we have found that the 1<
sym05> cell specific expression of
apx-1 is dependent on
lin-1, an Ets gene. In addition, in
lin-1 mutants, adjacent VPCs often adopt the 1<
sym05> fate, indicating a failure of lateral signaling. Our results provide a possible molecular basis for a positive role of LIN-1 in VPC specification: phosphorylation of LIN-1 by MAPK may convert LIN-1 into a transcriptional activator (see also Howard and Sundaram, 2002). References:Chen, N. and Greenwald, I. (2004). The lateral signal for LIN-12/Notch in C. elegans vulval development comprises redundant secreted and transmembrane DSL proteins. Dev Cell 6, 183-92. Howard, R. M. and Sundaram, M. V. (2002). C. elegans EOR-1/PLZF and EOR-2 positively regulate Ras and Wnt signaling and function redundantly with LIN-25 and the SUR-2 Mediator component. Genes Dev 16, 1815-27.