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Cloning and characterization of two neural‐salient serine/arginine‐rich (NSSR) proteins involved in the regulation of alternative splicing in neurones
Author(s) -
Komatsu Masaaki,
Kominami Eiki,
Arahata Kiichi,
Tsukahara Toshifumi
Publication year - 1999
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1046/j.1365-2443.1999.00286.x
Subject(s) - alternative splicing , biology , rna splicing , exon , sr protein , exon skipping , ribonucleoprotein , microbiology and biotechnology , splicing factor , gene , genetics , rna
Background In neurones, alternative splicing regulates the functions of many gene products. However, the molecular basis of neural‐specific splicing, and how splicing regulation is modulated in different neurones remains to be determined. Results We cloned two new SR proteins, Neural‐salient SR proteins (NSSR) 1 and 2, which are present at higher levels in brain and testis. During the differentiation, NSSR 1 is detected only in the neuronal stage. Both the purified recombinant NSSR 1 and 2 proteins enhance the in vitro splicing activity of nuclear extract. Moreover, recombinant NSSR 1 protein enhances the assembly of ribonucleoprotein complexes with S100 fraction. Over‐expression of NSSR 2 prevents the inclusion of either the Flip or Flop exons in the splicing of the GluR‐B gene, resulting in an increase in the abnormal exon‐skipping product. In contrast, transient transfection with NSSR 1 promotes the inclusion of the Flip exon so that the abnormal product is spliced to the mature spliced form. This suppression of exon skipping by NSSR 1 is observed even with co‐transfection of NSSR 2. Conclusions NSSR 1 and 2 were cloned from mouse cDNA libraries. Results indicate that NSSR 1 may play a crucial role in the regulation of alternative splicing in neurones.