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Molecular and Cellular Biology, March 1999, p. 2308-2321, Vol. 19, No. 3
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Down-Regulation of RpS21, a Putative Translation Initiation
Factor Interacting with P40, Produces Viable Minute Imagos and
Larval Lethality with Overgrown Hematopoietic Organs and
Imaginal Discs
István
Török,1
Daniela
Herrmann-Horle,1
István
Kiss,2
Gabriela
Tick,2
Gábor
Speer,1,
Rolf
Schmitt,1 and
Bernard
M.
Mechler1,*
Department of Developmental Genetics,
Deutsches Krebsforschungszentrum, D-69120 Heidelberg,
Germany,1 and Institute of Genetics,
Biological Research Center of the Hungarian Academy of
Sciences, H-6701 Szeged, Hungary2
Received 27 August 1998/Returned for modification 27 October
1998/Accepted 7 December 1998
Down-regulation of the Drosophila ribosomal protein S21
gene (rpS21) causes a dominant weak Minute
phenotype 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.
*
Corresponding author. Mailing address: Department of
Developmental Genetics, Deutsches Krebsforschungszentrum, Im
Neuenheimer Feld 280, D-69120 Heidelberg, Germany. Phone:
49-6221-424502. Fax: 49-6221-424552. E-mail:
dev.genetics{at}dkfz-heidelberg.de.

Present address: First Department of Medicine, Semmelweis
University Medical School, H-1083 Budapest,
Hungary.
Molecular and Cellular Biology, March 1999, p. 2308-2321, Vol. 19, No. 3
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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