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 TfIId+
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
cdc 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 cdc
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 cdc phenotype. These results
suggest that the cdc phenotype in prp12-1 is caused
by a selective reduction of spliced transcripts encoding a protein
(or proteins) required for G2/M transition.