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Molecular and Cellular Biology, April 2007, p. 3087-3097, Vol. 27, No. 8
0270-7306/07/$08.00+0 doi:10.1128/MCB.01876-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
,
Jérôme Dejardin,2,
Jamal Tazi,1* and
Johann Soret1*
CNRS, UMR 5535, Institut de Génétique Moléculaire de Montpellier, Montpellier F-34293, France,1 CNRS, UPR 1142, Institut de Génétique Humaine, CNRS, Montpellier F-34293, France2
Received 5 October 2006/ Returned for modification 9 November 2006/ Accepted 18 January 2007
Deciphering the role of alternative splicing in developmental processes relies on the identification of key genes whose expression is controlled by splicing regulators throughout the growth of a whole organism. Modulating the expression levels of five SR proteins in the developing eye of Drosophila melanogaster revealed that these splicing factors induce various phenotypic alterations in eye organogenesis and also affect viability. Although the SR proteins dASF/SF2 and B52 caused defects in ommatidia structure, only B52 impaired normal axonal projections of photoreceptors and neurogenesis in visual ganglia. Microarray analyses revealed that many transcripts involved in brain organogenesis have altered splicing profiles upon both loss and gain of B52 function. Conversely, a large proportion of transcripts regulated by dASF/SF2 are involved in eye development. These differential and specific effects of SR proteins indicate that they function to confer accuracy to developmental gene expression programs by facilitating the cell lineage decisions that underline the generation of tissue identities.
Published ahead of print on 5 February 2007.
Supplemental material for this article may be found at http://mcb.asm.org/.
Present address: Donnelly Centre for Cellular and Biomolecular Research, University of Toronto, Toronto, Canada M5S 3E1.
Present address: Harvard Medical School, Department of Genetics, and Massachusetts General Hospital, Department of Molecular Biology, Boston, MA 02114.
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