dictyNews Electronic Edition Volume 37, number 9 October 14, 2011 Please submit abstracts of your papers as soon as they have been accepted for publication by sending them to dicty@northwestern.edu or by using the form at http://dictybase.org/db/cgi-bin/dictyBase/abstract_submit. Back issues of dictyNews, the Dicty Reference database and other useful information is available at dictyBase - http://dictybase.org. Follow dictyBase on twitter: http://twitter.com/dictybase ========= Abstracts ========= DPKC-mediated ZYG1 phosphorylation induces fusion of myoblasts as well as of Dictyostelium cells Aiko Amagai1*, Harry MacWilliams2, Takahiro Isono3, Mariko Omatsu-Kanbe4, Shinya Urano1, Kazuo Yamamoto1,Yasuo Maeda1 1Graduate School of Life Sciences, Tohoku University, Sendai 980-8577, Japan, 2Zoologisch, Institute, Ludwig-Maximilians Universitat, Luisenstr., 14, 80333, MÙnchen, Germany, 3Central Research Laboratory, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan, 4Department of Physiology, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan International Journal of Cell Biology, in press We have previously demonstrated that a novel protein ZYG1 induces sexual cell fusion (zygote formation) of Dictyostelium cells [1]. In the process of cell fusion, involvements of signal transduction pathways via Ca2+ and PKC (protein kinase C) have been suggested because zygote formation is greatly enhanced by PKC activators [2-6]. In fact, there are several deduced sites phosphorylated by PKC in ZYG1 protein [1]. Thereupon, we designed the present work to examine whether or not ZYG1 is actually phosphorylated by PKC and localized at the regions of cell-cell contact where cell fusion occurs. These were ascertained, suggesting that ZYG1 might be the target protein for PKC. Since the signaling pathway via Ca2+ and PKC is also known to be involved in myoblast fusion as well as in Dictyostelium cell fusion [7-11], we have interested to know if there is a functionally ZYG1-like protein capable of inducing cell fusion in myoblasts. For this, a humanized version of zyg1 cDNA (mzyg1) was introduced into myoblasts to know if ZYG1 is also effective in cell fusion of myoblasts. Quite interestingly, enforced expression of ZYG1 in myoblasts was found to induce markedly their cell fusion, thus strongly suggesting the existence of a common signaling pathway for cell fusion beyond the difference of species. Submitted by: Aiko Amagai [aiamagai@amber.plala.or.jp] -------------------------------------------------------------------------------- Different Modes of State Transitions Determine Pattern in the Phosphatidylinositide-Actin System Gunther Gerisch1*, Mary Ecke1, Dirk Wischnewski1, and Britta Schroth-Diez2 1Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany 2Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstrasse 108, 01307 Dresden, Germany BMC Cell Biology, accepted Background In a motile polarized cell the actin system is differentiated to allow protrusion at the front and retraction at the tail. This differentiation is linked to the phosphoinositide pattern in the plasma membrane. In the highly motile Dictyostelium cells studied here, the front is dominated by PI3-kinases producing PI(3,4,5)tris-phosphate (PIP3), the tail by the PI3-phosphatase PTEN that hydrolyses PIP3 to PI(4,5)bis-phosphate. To study de-novo cell polarization, we first depolymerized actin and subsequently recorded the spontaneous reorganization of actin patterns in relation to PTEN. Results In a transient stage of recovery from depolymerization, symmetric actin patterns alternate periodically with asymmetric ones. The switches to asymmetry coincide with the unilateral membrane-binding of PTEN. The modes of state transitions in the actin and PTEN systems differ. Transitions in the actin system propagate as waves that are initiated at single sites by the amplification of spontaneous fluctuations. In PTEN-null cells, these waves still propagate with normal speed but loose their regular periodicity. Membrane-binding of PTEN is induced at the border of a coherent PTEN- rich area in the form of expanding and regressing gradients. Conclusions The state transitions in actin organization and the reversible transition from cytoplasmic to membrane-bound PTEN are synchronized but their patterns differ. The transitions in actin organization are independent of PTEN, but when PTEN is present, they are coupled to periodic changes in the membrane-binding of this PIP3-degrading phosphatase. The PTEN oscillations are related to motility patterns of chemotaxing cells. Submitted by: Gunther Gerisch [gerisch@biochem.mpg.de] ============================================================== [End dictyNews, volume 37, number 9]