Abstract
Down-regulation of the Drosophila ribosomal protein S21 gene (rpS21) causes a dominant weak Minutephenotype and recessively produces massive hyperplasia of the hematopoietic organs and moderate overgrowth of the imaginal discs during larval development. Here, we show that the S21 protein (RpS21) is bound to native 40S ribosomal subunits in a salt-labile association and is absent from polysomes, indicating that it acts as a translation initiation factor rather than as a core ribosomal protein. RpS21 can interact strongly with P40, a ribosomal peripheral protein encoded by the stubarista(sta) gene. Genetic studies reveal that P40 underexpression drastically enhances imaginal disc overgrowth in rpS21-deficient larvae, whereas viable combinations between rpS21 and sta affect the morphology of bristles, antennae, and aristae. These data demonstrate a strong interaction between components of the translation machinery and showed that their underexpression impairs the control of cell proliferation in both hematopoietic organs and imaginal discs.
ACKNOWLEDGMENTS
We thank Andrew Lambertsson for his help in the preliminary characterization of the Minute phenotype.
This work was supported by grants of the Deutsche Forschungsgemeindschaft (436UNG113/81/0) within the framework of a German-Hungarian program of scientific cooperation, the European Commission Biomed Programme (BMH1-CT94-1572) and Biotechnology Programme (BIO4-CT95-0202), a grant given to I.K. by the Hungarian Scientific Research Fund (OTKA T166/93), and an International Research Scholar’s award from the Howard Hughes Medical Institute given to I.K. and B.M.M.