The SR family proteins B52 and dASF/SF2 modulate development of the Drosophila visual system by regulating specific RNA targets

Gabut, M.; Dejardin, J.; Tazi, J.; Soret, J.

Mol Cell Biol

2007-04 / vol 27 / pages 3087-97


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.

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Female; Animals; Male; Drosophila Proteins/genetics/*metabolism; Phenotype; RNA Splicing/genetics; Immunoprecipitation; Reverse Transcriptase Polymerase Chain Reaction; Oligonucleotide Array Sequence Analysis; Cell Survival; Reproducibility of Results; RNA, Messenger/genetics/metabolism; Morphogenesis; Recombinant Fusion Proteins/metabolism; Nuclear Proteins/*metabolism; RNA-Binding Proteins/genetics/*metabolism; Phosphoproteins/*metabolism; Animals, Genetically Modified; Brain/growth & development/metabolism; Drosophila melanogaster/genetics/*growth & development; Eye/cytology/*growth & development/metabolism; Genes, Developmental; Genes, Insect; Larva/cytology; Photoreceptors, Invertebrate/cytology/metabolism

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