CSM News Electronic Edition Volume 3, number 3 July 16, 1994 Please submit abstracts of your papers as soon as they have been accepted for publication by sending them to CSM-News@worms.cmsbio.nwu.edu. Back issues of CSM-News, the CSM Reference database and other useful information is available by anonymous ftp from worms.cmsbio.nwu.edu [165.124.233.50], via Gopher at the same address, or by World Wide Web through www.nwu.edu. =========== Abstracts =========== Identification and Functional Analysis of a Developmentally Regulated ERK Gene in Dictyostelium discoideum Chris Gaskins, Mineko Maeda, and Richard A. Firtel Department of Biology, Center for Molecular Genetics, University of California, San Diego, La Jolla, California 92093-0634, telephone: 619-534-2788, fax: 619-534-7073 MOLECULAR AND CELLULAR BIOLOGY, IN PRESS ABSTRACT We have cloned a developmentally regulated MAP kinase (ERK) from Dictyostelium designated ERK1. Using anti-pTyr antibodies, we show that ERK1 is phosphorylated on tyrosine in vivo and that it will phosphorylate myelin basic protein. The gene expresses two transcripts, one that is preferentially expressed during vegetative growth and early development and one that is induced during the mutlicellular stages. Developmental Western blots using anti-ERK1 antibodies indicate ERK1 is present throughout development. ERK1/lacZ reporter constructs suggest that in the multicellular stages, the gene is preferentially expressed in a sub-population of cells scattered through the organism, similar to the pattern seen with anterior-like cell markers. Antisense mutagenesis from a derepressable promoter indicates ERK1 is essential for vegetative growth. Overexpression of ERK1 from either the Actin 15 promoter or the ERK1 promoter results in abnormal morphogenesis starting at the slug stage. Overexpression of ERK1 in null mutants of the phosphotyrosine phosphatase PTP2 results in the production of large aggregation streams and subsequent abnormal morphogenesis that indicates a genetic interaction between ERK1 and PTP2. These cells produce very large aggregation streams that break up into very small mounds that undergo abnormal morphogenesis. The genetic interaction between ERK1 and PTP2 appears to be specific since overexpression of ERK1 in a ptp1- null mutant does not produce the same phenotype. Our results indicate that ERK1 plays an essential role during the growth and differentiation of Dictyostelium. ------------------------------------------------------------------- [End CSM-News. volume 3, number 3]