Effect of drugs on lipid methylation,receptor-adenylate cyclase coupling and cyclic AMP secretion in Dictyostelium discoideum |
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| Affiliation: | 1. Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul 110-799, Republic of Korea;2. Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 110-799, Republic of Korea;3. Department of Physiology, Seoul National University College of Medicine, Seoul 110-799, Republic of Korea;1. Alberta Children’s Hospital Research Institute, University of Calgary, Canada;2. Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Canada;1. Programa de Processos Tecnológicos e Ambientais, Universidade de Sorocaba (UNISO), Sorocaba, SP, Brazil;2. Laboratório Nacional de Biociências (LNBio), Centro Nacional de Pesquisa em Energia e Materiais (CNPEM), Campinas, São Paulo, Brazil;3. Department of Biological and Chemical Engineering (BCE), Aarhus University, Aarhus, Denmark;4. Institute of Microbiology and Infection, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom;5. Centro de Ciências Naturais e Humanas, Universidade Federal do ABC (UFABC), Santo André, São Paulo, Brazil;6. Laboratório Nacional de Luz Sincrotron (LNLS), Centro Nacional de Pesquisa em Energia e Materiais (CNPEM), Campinas, São Paulo, Brazil;7. Institute for Cell and Molecular Biosciences, The Medical School, Newcastle University, Newcastle, United Kingdom |
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| Abstract: | Intercellular communication in Dictyostelium discoideum takes place by means of cyclic AMP-induced cyclic AMP-synthesis and secretion. Since phospholipid methylation has been suggested to play a role in receptor-adenylate cyclase coupling, we examined the effects of transmethylation inhibitors on the production of cyclic AMP during slime mold chemotaxis. Although cycloleucine and l-homocysteic acid were able to inhibit phospholipid methylation and nonpolar lipid methylation up to 40%, these drugs did not cause any decrease of receptor-mediated cAMP-synthesis and secretion. l-Homocysteine thiolactone and dl-homocysteine did not slow down the initial rate of receptor-mediated cAMP-synthesis, but both drugs retarded cAMP-secretion by about 50–75%. Yet, homocysteine thiolactone caused no significant decrease of phospholipid methylation, whereas homocysteine depressed the incorporation of methyl groups into phospholipid up to 80%. Treatment of aggregative cells with 0.1% n-butanol (v/v) resulted in a 3-fold stimulation of phospholipid methylation, whereas nonpolar lipid methylation and cAMP-synthesis were unaffected and cAMP-secretion showed a 2-fold decrease. It is concluded that no direct relationship exists between lipid methylation and receptor-adenylate cyclase coupling or lipid methylation and cAMP-secretion. Homocysteine thiolactone, homocysteine and butanol appear to affect secretion by a mechanism which involves factors other than lipid methylation. |
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