期刊论文详细信息
BMC Developmental Biology
Ectopic expression of cyclase associated protein CAP restores the streaming and aggregation defects of adenylyl cyclase a deficient Dictyostelium discoideum cells
Angelika A Noegel5  Michael Schleicher2  Rosemarie Blau-Wasser4  Francisco Rivero1  Girish Neelakanta3  Hameeda Sultana3 
[1] Centre for Cardiovascular and Metabolic Research, The Hull York Medical School and Department of Biological Sciences, University of Hull, Hull HU6 7RX, UK;Institute for Anatomy and Cell Biology, Ludwig-Maximilians-Universität, 80336 München, Germany;Section of Infectious Diseases, Department of Internal Medicine, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06520, USA;Center for Biochemistry, Medical Faculty, University of Cologne, 50931 Köln, Germany;Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Köln, Germany
关键词: Adenylyl cyclase ACB;    Adenylyl cyclase ACA;    Cyclase associated protein;    development;    cell-adhesion;    aggregation;    Cell polarity;   
Others  :  1086830
DOI  :  10.1186/1471-213X-12-3
 received in 2011-08-17, accepted in 2012-01-12,  发布年份 2012
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【 摘 要 】

Background

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.

Results

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.

Conclusions

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.

【 授权许可】

   
2012 Sultana et al; licensee BioMed Central Ltd.

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