Open Access Research article

Ectopic expression of cyclase associated protein CAP restores the streaming and aggregation defects of adenylyl cyclase a deficient Dictyostelium discoideum cells

Hameeda Sultana12*, Girish Neelakanta2, Francisco Rivero3, Rosemarie Blau-Wasser1, Michael Schleicher4 and Angelika A Noegel156*

Author Affiliations

1 Center for Biochemistry, Medical Faculty, University of Cologne, 50931 Köln, Germany

2 Section of Infectious Diseases, Department of Internal Medicine, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06520, USA

3 Centre for Cardiovascular and Metabolic Research, The Hull York Medical School and Department of Biological Sciences, University of Hull, Hull HU6 7RX, UK

4 Institute for Anatomy and Cell Biology, Ludwig-Maximilians-Universität, 80336 München, Germany

5 Center for Molecular Medicine Cologne (CMMC), University of Cologne, 50931 Köln, Germany

6 Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Köln, Germany

For all author emails, please log on.

BMC Developmental Biology 2012, 12:3  doi:10.1186/1471-213X-12-3

Published: 12 January 2012



Cell adhesion, an integral part of D. discoideum development, is important for morphogenesis and regulated gene expression in the multicellular context and is required to trigger cell-differentiation. G-protein linked adenylyl cyclase pathways are crucially involved and a mutant lacking the aggregation specific adenylyl cyclase ACA does not undergo multicellular development.


Here, we have investigated the role of cyclase-associated protein (CAP), an important regulator of cell polarity and F-actin/G-actin ratio in the aca- mutant. We show that ectopic expression of GFP-CAP improves cell polarization, streaming and aggregation in aca- cells, but it fails to completely restore development. Our studies indicate a requirement of CAP in the ACA dependent signal transduction for progression of the development of unicellular amoebae into multicellular structures. The reduced expression of the cell adhesion molecule DdCAD1 together with csA is responsible for the defects in aca- cells to initiate multicellular development. Early development was restored by the expression of GFP-CAP that enhanced the DdCAD1 transcript levels and to a lesser extent the csA mRNA levels.


Collectively, our data shows a novel role of CAP in regulating cell adhesion mechanisms during development that might be envisioned to unravel the functions of mammalian CAP during animal embryogenesis.

Cell polarity; aggregation; cell-adhesion; development; Cyclase associated protein; Adenylyl cyclase ACA; Adenylyl cyclase ACB