REGULATION OF DICTYOSTELIUM MORPHOGENESIS BY CAMP-DEPENDENT PROTEIN-KINASE

Citation
Jg. Williams et al., REGULATION OF DICTYOSTELIUM MORPHOGENESIS BY CAMP-DEPENDENT PROTEIN-KINASE, Philosophical transactions-Royal Society of London. Biological sciences, 340(1293), 1993, pp. 305-313
Citations number
77
Categorie Soggetti
Biology
ISSN journal
09628436
Volume
340
Issue
1293
Year of publication
1993
Pages
305 - 313
Database
ISI
SICI code
0962-8436(1993)340:1293<305:RODMBC>2.0.ZU;2-O
Abstract
During formation of the Dictyostelium slug extracellular cAMP signals direct the differentiation of prespore cells and DIF, a chlorinated he xaphenone, induces the differentiation of prestalk cells. At culminati on the slug transforms into a fruiting body, composed of a stalk suppo rting a ball of spores. A dominant inhibitor of cAMP-dependent protein kinase (PKA) expressed under the control of a prestalk-specific promo ter blocks the differentiation of prestalk cells into stalk cells. Ana lysis of a gene specifically expressed in stalk cells suggests that PK A acts to remove a repressor that prevents the premature induction of stalk cell differentiation by DIF during slug migration. PKA is also n ecessary for the morphogenetic movement of prestalk cells at culminati on. Expression of the PKA inhibitor under control of a prespore-specif ic promoter blocks the accumulation of prespore mRNA sequences and pre vents terminal spore cell differentiation. Thus PKA is essential for p rogression along both pathways of terminal differentiation but with di fferent mechanisms of action. On the stalk cell pathway it acts to reg ulate the action of DIF while on the spore cell pathway PKA itself see ms to act as the inducer of spore cell maturation. Ammonia, the extrac ellular signal which regulates the entry into culmination, acts by con trolling the intracellular concentration of cAMP and thus exerts its e ffects via PKA. The fact that PKA is necessary for both prespore and s pore gene expression leads us to postulate the existence of a signalli ng mechanism which converts the progressive rise in cAMP concentration during development into discrete, PKA-regulated gene activation event s.