Patterning in Dictyostelium illustrates a poorly understood mechanism, in which cells differentiate scattered amongst other cell types in response to a diffusible signaling molecule (DIF) before sorting into discrete tissues. DIF promotes a set of transcription factors to the move to nucleus where they activate or repress target gene expression. However, little is known about the molecular mechanism leading to transcription factor activation. Subsequent patterning of the cell types is driven by differential cell adhesion and cell motility. Again, little is known about the molecules that regulate these processes. We use genetics, biochemistry and microarrays to identify novel components of the DIF signaling pathway and regulators of cell adhesion and motility.
During Dictyostelium development, 20% of the cells die to make a cellular stalk. This represents a problem of altruism and cheater control: since stalk cells sacrifice themselves to aid spore dispersal, what prevents the emergence of cheaters that gain the benefit without paying their fair share of the cost? We study lab generated cheater and loser mutants and genes to define the pathways that control cell fate choice and social behaviour.
P2X receptors are ATP gated ion channels that regulate responses to extracellular ATP. However, we recently discovered an intracellular function for a P2X receptor in Dictyostelium, thus raising new questions about their role and regulation. In addition, several other Dictyostelium P2X receptors exist and little is known about the regulation of P2X receptors or their downstream effectors in any organism. We are using the genetic, proteomic and post-genomic tools available in Dictyostelium to address these questions.
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