ABSTRACT
We have identified a gene (PslA) that is expressed throughout Dictyostelium development and encodes a novel protein that is required for proper aggregation and subsequent cell-type differentiation and morphogenesis. pslA null (pslA−) cells produce large aggregation streams under conditions in which wild-type cells form discrete aggregates. Tips form along the stream, elongate to produce a finger, and eventually form a terminal structure that lacks a true sorus (spore head). More than half of the cells remain as a mass at the base of the developing fingers. The primary defect in the pslA− strain is the inability to induce prespore cell differentiation. Analyses of gene expression show a complete lack of prespore- specific gene expression and no mature spores are produced. In chimeras with wild-type cells, pslA− cells form the prestalk domain and normal, properly proportioned fruiting bodies can be produced. This indicates that pslA− cells are able to interact with wild- type cells and regulate patterning, even though pslA− cells are unable to express prespore cell-type-specific genes, do not participate in prespore cell differentiation and do not produce pslA− spores in the chimeras. While pslA− cells produce mature, vacuolated stalk cells during multicellular development, pslA− cells are unable to do so in vitro in response to exogenous DIF (a morphogen required for prestalk and stalk cell differentiation). These results indicate that pslA− cells exhibit a defect in the prestalk/stalk cell pathways under these experimental conditions. Our results suggest that PslA’s primary function is to regulate prespore cell determination very early in the prespore pathway via a cell-autonomous mechanism, possibly at the time of the initial prestalk/prespore cell-fate decision. Indirect immunofluorescence of myc-tagged PslA localizes the protein to the nucleus, suggesting that PslA may function to control the prespore pathway at the level of transcription.