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The alternative splicing factor PSI regulates P-element third intron splicing in vivo
M D Adams1, R S Tarng, D C Rio
1Department of Molecular and Cell Biology, University of California, Berkeley 94720-3204, USA.
Genes & Development
|January 1, 1997
Summary
The P-element somatic inhibitor (PSI) protein prevents P-element intron splicing in Drosophila somatic cells. Ectopic PSI expression in the germ line represses splicing, confirming PSI
Area of Science:
- Molecular Biology
- Genetics
- Developmental Biology
Background:
- Drosophila P-element transposition is restricted to the germ line.
- Somatic P-element intron splicing is inhibited by a multiprotein complex.
- This complex binds a regulatory sequence in the third intron's 5' exon.
Purpose of the Study:
- To investigate the role of the P-element somatic inhibitor (PSI) protein in regulating P-element intron splicing.
- To determine if PSI is sufficient to inhibit splicing in the germ line.
- To confirm PSI's function as a tissue-specific splicing regulator.
Main Methods:
- In vitro splicing assays using purified components.
- Transgenic Drosophila expressing reporter constructs.
- Ectopic expression of PSI in the female germ line.
- Antisense ribozyme experiments in somatic cells.
Main Results:
- PSI is a necessary component for inhibiting IVS3 splicing in vitro.
- Ectopic germ line expression of PSI repressed IVS3 reporter transgene splicing.
- Antisense PSI ribozymes activated IVS3 splicing in somatic cells.
Conclusions:
- PSI acts as a key tissue-specific regulator of P-element third intron splicing.
- PSI's soma-specific expression pattern explains the restriction of P-element transposition to the germ line.
- PSI mediates somatic inhibition of splicing through a ribonucleoprotein complex.