Dictyostelium DIF-1 response and prestalk gene activation

The transcriptional response to the morphogen DIF-1 that specifies prestalk/ stalk cell fate in Dictyostelium discoideum. DIF-1 (the chlorinated acylphloroglucinol produced by the dicty_dif1_biosynthesis module) is perceived by the basic-region leucine-zipper (bZIP) transcription factors DimA and DimB, which translocate to the nucleus and reprogram cell-type gene expression: DimA/DimB activate prestalk/stalk genes (the extracellular-matrix markers ecmA and ecmB) and repress prespore genes, so a cell exposed to DIF-1 commits to the prestalk pathway. The two bZIPs are partly redundant and heterodimerise, with DimB the principal activator of ecmB. This module is the RESPONSE arm; its input is the DIF-1 made by the separate biosynthesis module. OUT OF SCOPE: DIF-1 biosynthesis (dicty_dif1_biosynthesis module), the STATa/CudA culmination circuit (CudA is only indirectly DIF-1-linked), and DIF-1 catabolism. Phrased over transcription-factor functions and family selectors with D. discoideum representatives.

Dictyostelium-specific developmental patterning module (the DIF-1 RESPONSE arm) grounded to the two bZIP transcription factors DimA (Q54XG7) and DimB (Q54ER9) and their extracellular-matrix output markers EcmA (Q54YG2) and EcmB (P11976). Paired with dicty_dif1_biosynthesis (which produces the DIF-1 input). CudA is intentionally excluded (it acts mainly downstream of STATa in culmination, not as a direct DIF-1 effector). GO molecular-function terms were taken from the completed DICDI reviews; nodes use PANTHER family selectors plus D. discoideum representative members. Named to signal Dictyostelium scope. STATc is a second, parallel DIF-1 effector (it restricts ecmA while DimA/DimB induce it), and the STATa/CudA culmination circuit excluded here is the STATa variant of dicty_jak_independent_stat_signaling, which models both STAT arms.