CSM News Electronic Edition Volume 2, number 11 March 12, 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 [129.105.233.50], via Gopher at the same address, or by World Wide Web through WWW.acns.nwu.edu. --------------------------- Post-doc Position Available --------------------------- Postdoctoral fellowships available in two collaborating laboratories, which study cell motility of Dictyostelium, especially the role of actin and myosin. A wide variety of molecular, cellular and biochphysical techniques are available, both in our laboratories and in laboratories of colleagues on campus. Contact either of us at Washington University in St. Louis. John Cooper Dept. of Cell Biology & Physiology jcooper@cellbio.wustl.edu Elliot Elson Dept. of Biochemistry & Molecular Biophysics elson_e@biochm.wustl.edu --------- Abstracts --------- LagC is required for cell-cell interactions that are essential for cell-type differentiation in Dictyostelium Joseph L. Dynes, Alexandra M. Clark, Gad Shaulsky, Adam Kuspa, William F. Loomis, and Richard A. Firtel1 Department of Biology Center for Molecular Genetics University of California, San Diego 9500 Gilman Drive La Jolla, CA 92093-0634 1 To whom correspondence should be addressed at: Center for Molecular Genetics, Room 225, University of California, San Diego, 9500 Gilman Drive La Jolla, CA 92093-0634 tel. (619) 534-2788 fax (619) 534-7073 ACCEPTED FOR PUBLICATION: GENES AND DEVELOPMENT. VOL. 8; ISSUE 8 (SECOND ISSUE, APRIL) Abstract Strain AK127 is a developmental mutant of Dictyostelium discoideum that was isolated by restriction enzyme mediated integration (REMI). Mutant cells aggregate normally but are unable to proceed past the loose aggregate stage. The cloned gene, (loose aggregate C) lagC, encodes a novel protein of 98 kDal that contains an N-terminal signal sequence and a putative C-terminal transmembrane domain. The mutant strain AK127 shows no detectable lagC transcript upon Northern analysis, indicating that the observed phenotype is that of a null allele. Expression of the lagC cDNA in AK127 cells complements the arrest at the loose aggregate stage, indicating that the mutant phenotype results from disruption of the lagC gene. In wild-type cells, lagC mRNA is induced at the loose aggregate stage and is expressed through the remainder of development. lagC- null cells aggregate, but then disaggregate and reaggregate to form small granular mounds. Mature spores are produced at an extremely low efficiency (< 0.1% of wild type), appearing only after ~72 hr, while wild-type strains produce mature spores by 26 hr. lagC- null cells accumulate reduced levels of transcripts for the prestalk-enriched genes rasD and CP2, and do not express the DIF-induced prestalk-specific gene ecmA or the cAMP-induced prespore-specific gene SP60 to significant levels. In chimeric organisms resulting from the co-aggregation of lagC- null and wild-type cells, cell-type-specific gene expression is rescued in the lagC- null cells; however, lagC- prespore cells are localized to the posterior of the prespore region and do not form mature spores, suggesting that LagC protein has both cell non-autonomous and cell autonomous functions. Overexpression of lagC from an actin promoter in both wild-type and lagC- cells causes a delay at the tight aggregate stage, the first stage requiring LagC activity. These results suggests that the LagC protein functions as a non-diffusible cell-cell signaling molecule that is required for multicellular development. ------------------------------------------------------------------------- [End CSM News, Issue 2, Volume 11]