TY - JOUR
T1 - The Saccharomyces cerevisiae gene CDC40/PRP17 controls cell cycle progression through splicing of the ANC1 gene
AU - Dahan, Orna
AU - Kupiec, Martin
N1 - Funding Information:
We thank all members of the Kupiec group for support and ideas, especially Dr Sigal Ben Yehuda and Dr Orna Landman. We also thank D. Kornitzer, M. Ares, C. Guthrie and D. Drubin for reagents. This work was supported by grants to M.K. by AICR, ICRF and the Israeli Cancer Association.
PY - 2004
Y1 - 2004
N2 - The timing of events in the cell cycle is of crucial importance, as any error can lead to cell death or cancerous growth. This accurate timing is accomplished through the activation of specific CDC genes. Mutations in the CDC40/PRP17 gene cause cell cycle arrest at the G2/M stage. It was previously found that the CDC40 gene encodes a pre-mRNA splicing factor, which participates in the second step of the splicing reaction. In this paper we dissect the mechanism by which pre-mRNA splicing affects cell cycle progression. We identify ANC1 as the target of CDC40 regulation. Deletion of the ANC1 intron relieves the cell cycle arrest and temperature sensitivity of cdc40 mutants. Furthermore, we identify, through point mutation analysis, specific residues in the ANC1 intron that are important for its splicing dependency on Cdc40p. Our results demonstrate a novel mechanism of cell cycle regulation that relies on the differential splicing of a subset of introns by specific splicing factors.
AB - The timing of events in the cell cycle is of crucial importance, as any error can lead to cell death or cancerous growth. This accurate timing is accomplished through the activation of specific CDC genes. Mutations in the CDC40/PRP17 gene cause cell cycle arrest at the G2/M stage. It was previously found that the CDC40 gene encodes a pre-mRNA splicing factor, which participates in the second step of the splicing reaction. In this paper we dissect the mechanism by which pre-mRNA splicing affects cell cycle progression. We identify ANC1 as the target of CDC40 regulation. Deletion of the ANC1 intron relieves the cell cycle arrest and temperature sensitivity of cdc40 mutants. Furthermore, we identify, through point mutation analysis, specific residues in the ANC1 intron that are important for its splicing dependency on Cdc40p. Our results demonstrate a novel mechanism of cell cycle regulation that relies on the differential splicing of a subset of introns by specific splicing factors.
UR - http://www.scopus.com/inward/record.url?scp=2442712834&partnerID=8YFLogxK
U2 - 10.1093/nar/gkh574
DO - 10.1093/nar/gkh574
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
AN - SCOPUS:2442712834
SN - 0305-1048
VL - 32
SP - 2529
EP - 2540
JO - Nucleic Acids Research
JF - Nucleic Acids Research
IS - 8
ER -
