A cell-adhesion pathway regulates intercellular communication during Dictyostelium development.

Cell adhesion molecules play an important physical role in shaping the structure of multicellular organisms. Recent studies show that they also play a role in intracellular and intercellular signaling. We describe a cell adhesion pathway that is mediated by the intercellular communication genes comC, lagC, and lagD during Dictyostelium development. Disruptions of these genes result in strains that are unable to generate spores when developed in a pure population but are capable of sporulation when developed in chimerae with wild-type cells. In contrast, any pair-wise chimera of the three mutants fails to form spores. We postulate that the wild-type cells supply the mutant cells with a signal that partially rescues their sporulation. We also propose that the three mutants are deficient in the production of that signal, suggesting that the three genes function in one signaling pathway. In support of that notion, the mutant cells share common non-cell-autonomous prespore and prestalk-specific defects and a common pattern of developmental progression and regression. We provide transcriptional and functional evidence for a network in which comC inhibits lagC and activates lagD expression, lagC and lagD are mutually inductive, and the cell adhesion gene lagC is the terminal node in this signaling network.

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