Mutation of protein kinase A causes heterochronic development of Dictyostelium

In heterochronic mutants the relative timing of developmental events is altered compared with the wild type. This generally results in a disordered embryo, though heterochronic mutations may also be an important source of evolutionary variation. In the rapidly developing (rde) mutants of Dictyosteli...

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Bibliographic Details
Published in:	Nature (London) Vol. 356; no. 6365; pp. 171 - 172
Main Authors:	Simon, M.N, Pelegrini, O, Veron, M, Kay, R.R
Format:	Journal Article
Language:	English
Published:	London Nature Publishing 12-03-1992 Nature Publishing Group
Subjects:	Amino Acid Sequence Animals Base Sequence Biological and medical sciences Cell differentiation Cell Differentiation - genetics Classical genetics, quantitative genetics, hybrids cyclic AMP Cyclic AMP - physiology Dictyostelium Dictyostelium - enzymology Dictyostelium - genetics Dictyostelium - growth & development Fundamental and applied biological sciences. Psychology Genetics Genetics of eukaryotes. Biological and molecular evolution heterochronic mutants Inactivation Macromolecular Substances Molecular Sequence Data Morphogenesis Mutation Protein Kinases - chemistry Protein Kinases - genetics Proteins Protozoa Signal Transduction Protozoa Dictyostelium Enzymatic activity Enzyme Protein kinase Cyclic AMP Development Molecular interaction Mutation Mycetozoa
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Summary:	In heterochronic mutants the relative timing of developmental events is altered compared with the wild type. This generally results in a disordered embryo, though heterochronic mutations may also be an important source of evolutionary variation. In the rapidly developing (rde) mutants of Dictyostelium, stalk and spore cells differentiate before morphogenesis is complete. We have traced the lesion in one class of these mutants to the regulatory subunit of cyclic AMP-dependent protein kinase (pk-A). inactivation of this protein results in the unrestrained activity of the catalytic subunit, so prematurely triggering terminal cell differentiation.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0028-0836 1476-4687
DOI:	10.1038/356171a0