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#cell aggregation

2 public questions tagged with this topic.

Transition unicellular-multicellular regulated by:

Unicellular to multicellular transition is triggered by nutritional status rather than oxygen, pH, or temperature cues dominant in soil microenvironment. Decline in bacterial prey reduces intracellular amino acids and folate, decreasing TORC1 activity, activating YakA protein kinase, and permitting expression of early developmental proteins. Folate receptor downregulation and cAR1 upregulation switch chemotaxis preference from bacteria to cAMP. Nutrient depletion also induces autophagy providing metabolites for development without external food. Oxygen depletion would affect aeration but not initiate aggregation, pH increase and temperature drop are unreliable signals, making nutrient limitation authentic ecological trigger inducing survival morphogenesis and fruiting.

Ref: Nature, Dictyostelium starvation response - TOR downregulation and YakA activation triggering multicellular transition.

Adenylyl cyclase in aggregation:

Among three adenylyl cyclases, ACA encoded by acaA is uniquely required for aggregation signaling. Transcribed from multiple developmental promoters, ACA produces both extracellular cAMP for chemotactic relay and intracellular cAMP for PKA-dependent gene expression. Null acaA cells cannot generate cAMP oscillations, remain unable to aggregate, and fail to express early genes despite starvation. Exogenous pulses can rescue development. ACB encoded by acrA acts later during culmination, while ACG encoded by acgA functions as osmosensor controlling spore dormancy. ACP is not a Dictyostelium cyclase isoform, making ACA definitive aggregation-specific enzyme.

Ref: PLOS ONE, ACA adenylyl cyclase as aggregation cyclase - acaA alternative promoters and signal relay function.