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MBC in Press, published online ahead of print September 20, 2006
Mol. Biol. Cell 10.1091/mbc.E06-07-0619

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Submitted on July 21, 2006
Revised on August 28, 2006
Accepted on September 11, 2006

A Phg2-Adrm1 Pathway Participates in the Nutrient-controlled Developmental Response in Dictyostelium

Nathalie Cherix,* Romain Froquet,* Steve J. Charette,* Cédric Blanc,{dagger} François Letourneur,{dagger} and Pierre Cosson*

*Département de Physiologie et Métabolisme Cellulaire, Centre Médical Universitaire, Université de Genève, CH-1211 Genève 4, Switzerland; {dagger}Institut de Biologie et Chimie des Protéines, UMR 5086, CNRS/Université Lyon I, IFR 128 BioSciences Lyon-Gerland, F-69367 Lyon Cedex 07, France

Monitoring Editor: Carole Parent

Dictyostelium amoebae grow as single cells but upon starvation they initiate multicellular development. Phg2 was characterized previously as a kinase controlling cellular adhesion and the organization of the actin cytoskeleton. Here we report that Phg2 also plays a role during the transition between growth and multicellular development, as evidenced by the fact that phg2 mutant cells can initiate development even in the presence of nutrients. Even at low cell density and in rich medium, phg2 mutant cells express discoidin, one of the earliest pre-developmental markers. Complementation studies indicate that, in addition to the kinase domain, the core region of Phg2 is involved in the initiation of development. In this region, a small domain contiguous with a previously described ras-binding domain, was found to interact with the Dictyostelium ortholog of the mammalian adhesion-regulating molecule (ADRM1). In addition, adrm1 knockout cells also exhibit abnormal initiation of development. These results suggest that a Phg2-Adrm1 signaling pathway is involved in the control of the transition from growth to differentiation in Dictyostelium. Phg2 thus plays a dual role in the control of cellular adhesion and initiation of development.

Address correspondence to: Pierre Cosson (Pierre.Cosson{at}medecine.unige.ch)




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