Molecular and Cellular Biology, November 1999, p. 7846-7856, Vol. 19, No. 11
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Laboratoire de Génétique et Physiologie du Développement, UMR 6545 CNRS-Université, IBDM CNRS-INSERM-Université de la Méditerrannée, F-13288 Marseille Cedex 09, France
Received 28 April 1999/Returned for modification 7 June 1999/Accepted 14 July 1999
We have characterized the Drosophila bancal gene, which encodes a Drosophila homologue of the vertebrate hnRNP K protein. The bancal gene is essential for the correct size of adult appendages. Reduction of appendage size in bancal mutant flies appears to be due mainly to a reduction in the number of cell divisions in the imaginal discs. Transgenes expressing Drosophila or human hnRNP K are able to rescue weak bancal phenotype, showing the functional similarity of these proteins in vivo. High levels of either human or Drosophila hnRNP K protein in imaginal discs induces programmed cell death. Expression of the antiapoptotic P35 protein suppresses this phenotype in the eye, suggesting that apoptosis is the major cellular defect caused by overexpression of K protein. Finally, the human K protein acts as a negative regulator of bancal gene expression. We propose that negative autoregulation limits the level of Bancal protein produced in vivo.
Present address: Howard Hughes Medical Institute, Department of
Biochemistry and Biophysics, University of Pennsylvania School of
Medicine, Philadelphia, PA 19104-6148.
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