Ras effector switching as a developmental strategy.

摘要: Organisms pattern and specify cell fates with remarkably high fidelity robustness, cancer may be considered in part to a disease of fate specification gone awry. During C. elegans vulval development an initial EGF signal prompts Ras activate its canonical effector pathway, Raf-MEK-ERK, induce primary cell, which subsequently signals 2 neighbors via Notch develop as secondary cells. We have shown that signaling through alternate RalGEF-Ral, antagonizes Ras-Raf pro-primary signaling. Ras-RalGEF-Ral instead promotes support Notch. validated previous model can also contribute fate, argue mediates this pro-secondary activity. Ras-Raf-MEK-ERK was previously extinguished from cells by secondary-specific expression MAP kinase phosphatase, we found Ral is transcriptionally restricted Thus during R...