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A GAL4-SIR1 fusion gene was set under control of the constitutive promoter of the yeast alcohol dehydrogenase I, ADH1p [G. Ammerer, Methods Enzymol. 101, 192 (1983) ] in pRS316 (31). The GAL4-SIR1 fusion plasmid (pCF117) contained ADH1p (Bam Hl-Hind III from pJR1208), followed byGAL4-SIR1 (Hind III-Bgl II from pKL5 [C. Chien, P. L. Bartel, R. Sternglanz, S. Fields, Proc. Natl. Acad. Sci. U.S.A. 88, 9578 (1991)] containing the 5′ end of the gene} and the 3′ end of SIR1 including the SIR1 terminator (Bgl II-Hind III from pJR979).
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A GAL4-SIR1 fusion gene was set under control of the constitutive promoter of the yeast alcohol dehydrogenase I, ADH1p [G. Ammerer, Methods Enzymol. 101, 192 (1983) ] in pRS316 (31). The GAL4-SIR1 fusion plasmid (pCF117) contained ADH1p (Bam Hl-Hind III from pJR1208), followed byGAL4-SIR1 (Hind III-Bgl II from pKL5 [C. Chien, P. L. Bartel, R. Sternglanz, S. Fields, Proc. Natl. Acad. Sci. U.S.A. 88, 9578 (1991)] containing the 5′ end of the gene} and the 3′ end of SIR1 including the SIR1 terminator (Bgl II-Hind III from pJR979).
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Gal4 binding sites were introduced in place of the ACS of the synthetic HMR silencer (6). First, a Bam Hl-Sph I fragment containing the ACS was excised from pJR1273. pJR1273 consisted of the Eco Rl-Hind III fragment of HMR cloned into the Eco RI-Hind III sites of pUC18. This HMR allele also lacked HMR-I. In place of the excised ACS, annealed nucleotides that formed the Gal4 binding site were inserted (5′-GATCCCCCCTCGAGGATCTCGGAAGACTCTCCTCCGGCTGATGCATG-3′). Plasmids were screened for multiple insertions, and isolates that had one, three, and five tandem insertions (pJR1584, pJR1614, and pJR1619, respectively) were used to replace the nmrΔ::URA3 allele in JRY3933 (MATα ade2-1 his3-11,15 leu2-3,112 trp1-1 ura3-1 can1-100 hmrΔ::URA3) by one-step gene replacement [R. J. Rothstein, Methods Enzymol. 101, 202 (1983)]. Correct integration was verified by DNA blot hybridization.
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To create the Gal4-Orc2 and Gal4-Orc5 fusion proteins, we amplified the ORC2 and ORC5 open reading frames from yeast genomic DNA by polymerase chain reactions (PCR). The PCR primers used introduced Bam Hl sites both 5′ and 3′ of both genes. The PCR products were cleaved with Bam Hl and ligated into the Bam Hl site of pRH98-1, thus setting them under control of the constitutive glyceraldehyde dehydrogenase (GPD) promoter and the phosphoglycerate kinase (PGK) terminator. pRH98-1 is a derivative of YCplac33 [R. D. Gietz and A. Sugino, Gene 74, 527 (1988)), which has the Hind III-Xba I fragment of pG-1 [M. Schena, D. Picard, K. R. Yamamoto, Methods Enzymol. 194, 389 (1991)] containing a GPD-PGK cassette inserted at the Hind III and Xba I sites. The resulting plasmids, pJR1637 (expressing ORC2) and DJR1638 (expressing ORC5), were able to complement the temperature sensitivity and silencing defect of orc2-1 and orc5-1, respectively. Subsequently, a derivative of pRH98-1 was constructed that encoded the Gal4 DNA binding domain (residues 1 to 147). The GAL4 sequence was obtained by PCR amplification from yeast genomic DNA. The primers were designed such that a Bgl II site was generated 5′ and a Bam Hl site was created 3′ of the GAL4 sequence. The PCR product was cleaved with Bgl II and Bam Hl and inserted into the Bam Hl site of pRH98-1, between GPDp and PGK, generating pJR1639. Bam Hl fragments containing ORC2 (pJR1637) and ORC5 (pJR1638) were cloned into the unique Bam Hl site of pJR1639, generating the Gal4(1-147)-Orc2 (pJR1640) and Gal4(1-147)-Orc5 (pJR1641) fusion plasmids.
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note
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We thank D. Gottschling for constructs and the members of our laboratory for stimulating discussions. Supported by a grant from the National Institutes of Health (GM31105) (J.R.), by postdoctoral fellowships from the California Division of the American Cancer Society and the Leukemia Society of America (C.A.F.), by postdoctoral grants from the Swiss National Science Foundation and the Janggen-Pöhn Foundation (A.E.E.-M.), and by a Howard Hughes Medical Research Institute predoctoral fellowship (S.L.). C.A.F. thanks M. D. Sheets for discussion and support. Core support was provided by a National Institute of Environmental Health Sciences Mutagenesis Center grant to B. N. Ames.
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