dS6K regulated cell growth is dPKB/dPI3K independent, but requires dTOR and dPDK1. T. Radimerski ¹, J. Montagne ¹, F. Rintelen ², H. Stocker ², S. Oldham ², J. Van der Kaay ³, C.P. Downes ³, E. Hafen ², G. Thomas ¹. 1) Dept Growth Control, Friedrich Miescher Inst, Basel Stadt, Switzerland; 2) Zoology Institute, University of Zurich, Zurich, Switzerland; 3) Department of Life Sciences, University of Dundee, Dundee, Scotland.

   Several mutations in Drosophila delay development and affect organism size. Mutations in putative components of the insulin receptor (dInR) pathway have been shown to reduce cell size and cell number in a cell-autonomous fashion. Interestingly, null mutations in one such component, dS6K, affect only cell size but not cell number. To gain insights into the mechanisms that lead to dS6K activation a number of approaches were employed: (i) an enhancer-suppressor screen using a dS6K sensitized phenotype was carried out to identify novel genes that interact with dS6K (see poster of J. Montagne et al.), (ii) analysis of genetic interactions between dS6K and known components of the dInR pathway and (iii) biochemical and pharmacological approaches in both Drosophila cell culture and in staged Drosophila larvae were used to complement the genetic data. These studies led to the findings that dS6K activation is independent of dPKB and dPI3K activity but requires dTOR and dPDK1 signaling inputs. Moreover, dPI3K/dPKB driven growth is independent of dS6K, suggesting that dPKB and dS6K reside on parallel pathways.