2001年5月
Mutation in the prp12(+) gene encoding a homolog of SAP130/SF3b130 causes differential inhibition of pre-mRNA splicing and arrest of cell-cycle progression in Schizosaccharomyces pombe
RNA
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- 巻
- 7
- 号
- 5
- 開始ページ
- 671
- 終了ページ
- 681
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1017/S1355838201001200
- 出版者・発行元
- COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
prp12-1 is one of the mutants defective in pre-mRNA splicing at a nonpermissive temperature in Schizosaccharomyces pombe. We found that the prp12(+) gene encodes a protein highly homologous with a human splicing factor, SAP130/SF3b130, a subunit of a U2 snRNP-associated complex SF3b. Prp12p was shown to interact genetically with Prp10p that is a homolog of SAP155/SF3b155, another subunit in SF3b, suggesting that Prp12p is a functional homolog of human SAP130/SF3b130. Prp12p tagged with GFP is uniformly localized in the nuclear DNA region. In addition to pre-mRNA splicing defects, the prp12-1 mutant produced elongated cells, a typical phenotype of cell division cycle (cdc) mutants, suggesting a possible link between pre-mRNA splicing and cell-cycle progression. We examined kinetics of splicing defects in prp12-1 and several other prp mutants using northern blot hybridization and found that, among all the tested pre-mRNAs, only Tflld(+) pre-mRNA with low splicing efficiency showed detectable splicing defects at the nonpermissive temperature in prp12-1. In addition, we found that other prp mutants with the cde phenotype also showed differential splicing defects in tested pre-mRNAs at the nonpermissive temperature. On the other hand, prp mutants that do not exhibit the cde phenotype showed a rapid and complete block of pre-mRNA splicing in all the tested pre-mRNAs at the nonpermissive temperature, indicating that prp mutants with weak splicing defects have a tendency to exhibit the cde phenotype. These results suggest that the cde phenotype in prp12-1 is caused by a selective reduction of spliced transcripts encoding a protein (or proteins) required for G2/M transition.
- リンク情報
- ID情報
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- DOI : 10.1017/S1355838201001200
- ISSN : 1355-8382
- eISSN : 1469-9001
- Web of Science ID : WOS:000168500500003