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Molecular and Cellular Biology, November 1999, p. 7846-7856, Vol. 19, No. 11
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.
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
The Levels of the bancal Product, a
Drosophila Homologue of Vertebrate hnRNP K Protein, Affect
Cell Proliferation and Apoptosis in Imaginal Disc Cells

*
Corresponding author. Mailing address: LGPD-IBDM,
Université de la Méditerrannée, Campus de Luminy,
Case 907, 13288 Marseille Cedex 09, France. Phone: 33-4-9182-9424. Fax:
33-4-9182-0682. E-mail: vola{at}ibdm.univ-mrs.fr.
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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