Nuclear transcription factor with zinc-dependent sequence binding specificity. Required for carA-1 and carA-2 expression in early development. Also required throughout later developmental stages - where it has a cell-autonomous role that is distinct from its capacity to control carA-1 and carA-2 expression. Required for terminal spore differentiation but not essential for cell differentiation and cell sorting. May function to help insulate distinct pathways from simultaneous and universal activation by cAMP. Expressed throughout development. Up-regulated by P.aeruginosa, PAO1 strain and PA14 strain infection. Failure to develop under standard conditions and failure to induce expression of carA-1 and carA-2 early in development. Failure to sporulate, even under conditions that bypass the dependence on early cAMP signaling pathways. Do not form mature spores and all cells of the mutant spore mass are dark in phase with round or irregular shape. These cells are fragile and easily disrupted under a glass cover slip. Very low level of expression of carA-1 and carA-2 with resulting defects in cAMP signaling and thus impaired aggregation, although aggregates develop normally in the presence of a wild-type strain. Post-aggregation and sporulation defects are cell autonomous and independent of carA-1 expression. Early developmental events of CRTF-null strain can be rescued with exogenous cAMP treatment, constitutive carA-1 expression or co-development with wild-type cells; however, these treatments are insufficient to promote sporulation. In shaking culture, null cells grow with the same doubling time as wild-type cells and form normal size growth plaques on bacterial lawns; however, development within these plaques is very poor. When cells are developed directly on solid substrata, development of mutant cells is completely blocked prior to aggregation.