GENERAL CONCLUSION AND FUTURE WORK
7.3 Future work NER efficiency
The NER rate indicates that at the highly silenced chromosome ends, the repair time in the NTS and TS is approximately similar and more than 8 hrs. However, in the chromosome end where the silencing levels are low, there are marked differences between strands, the repair being faster at the TS compared to NTS. This suggests a transcriptional activity o f URA3 and the participation of TC-NER in the repair of TS. Furthermore, SIR2 deletion also impinges on NER efficiency, for example the NER efficiency was much faster at the TS of URA3 gene at the highly repressed end when
SIR2 is deleted. The involvement of the TC-NER in the TS of the NRE strain could be
tested by analysing the NER rate in the TS when RAD26 is deleted or mutated.
Telomeres have an equilibrium between Sir2p and its counterpart Sas2p histone acetyltransferase which acetylates predominantly histone H4K16, thus, the positions that Sir2p deacetylates (Suka et al., 2002). In this thesis it has been observed that deletion o f SIR2 influences the chromatin structure and NER rate, therefore it is likely that the deletion or mutation of SAS2 will impinge on NER efficiency and chromatin in subtelomeres.
Acetylation levels after UV and plasticity of the chromatin
NER efficiency depend on chromatin organisation since many studies have shown that at the NTS the repair rate is faster in the linker region and MNase accessible region compared to MNase resistant regions (Livingstone-Zatchej et al., 1997; Wellinger and Thoma, 1997). Nevertheless, the lesions in the protected regions might still be repaired due to nucleosome mobility (discussed in Chapter IV).
For example, chromatin studies have revealed the nucleosome positioning and MNase accessibility at the endogenous URA3 and when URA3 gene is inserted at a minichromosome. In both cases, the nucleosomal organisation is similar. This nucleosomal organisation at the URA3 gene is correlated with other studies of the NER efficiency analysis at the NTS of URA3 showing that the modulation of NER rate depends on the MNase accessibility (Tanaka et al., 1996; Thoma, 1986; Wellinger and Thoma, 1997).
In addition, the work presented here also suggests a correlation between the repair data and the MNase accessibility. For instance, in the RE, the MNase accessibility results suggest there is no regular nucleosome array, moreover, the repair
data provides evidence that the chromatin is probably highly compacted and even the linker regions are not accessible to the NER machinery. In the NRE, the chromatin is more accessible and NER efficiency is higher than at the RE strain; however the repair analysis and MNase accessibility at the NRE data also suggests that the chromatin follows an irregular pattern since there are no obvious changes in repair efficiency marking the linker regions or regions accessible to the NER machinery. Even when SIR2 is deleted at both NRE and RE, the repair analysis and MNase analysis suggested an irregular chromatin organisation.
The high resolution analysis of MNase accessibility alone cannot determine the nucleosome position or the precise chromatin organisation. Consequently, the low resolution nucleosome mapping together with high resolution MNase accessibility analysis could determine this issue.
In the RE, there was no evidence of an increase in acetylation levels after UV irradiation, however, in REs/r2A, NRE and NREs/r2A an increase in acetylation levels was detected after UV treatment. Previous studies have correlated acetylation with an “open” chromatin structure and transcription (Teng et al., 2002). Therefore, it can be speculated that after treatment with UV, the chromatin is reorganized in the REszV2A, NRE and NREs/r2A. To study this hypothesis, the accessibility of MNase to DNA after UV treatment could be examined. For example, in the REsz>2A strain, the MNase accessibility to DNA could be examined 60 mins after UV since the detected acetylation levels are the highest at that specific point.
Silenced regions and proteins
The S. cerevisiae genome has other silenced regions such as rDNA and HM loci. Therefore, NER can be also influenced in those regions and an analysis of them would broaden our knowledge of the silencing effect in NER.
There are other proteins, apart from Sir2p, that are involved in telomere silencing and each of them might influence NER differently. For example, a candidate protein could be Hdflp, the homologous of mammalian Ku70p also known as Yku70p, as silencing is affected when it is mutated (Pryde and Louis, 1999). Other candidate proteins could be Sir3p, Sir4p and Sirlp proteins as each o f them influence silencing differently. For example, in the subtelomeres, Sir2p and Sir4p completely abrogate silencing, Sir3p strongly reduces the level o f silencing whereas Sirlp causes only slight derepression (Pryde and Louis, 1999).
In addition, as previously mentioned in Chapter III, proteins that are directly involved in telomere length (such as riflp and ri£2p) are indirectly involved in silencing suggesting that they are good candidates to study whether they influence NER repair and chromatin structure.
Aboussekhra, A. et al. 1995. Mammalian DNA nucleotide excision repair reconstituted with purified protein components. Cell 80(6), pp. 859-868.
Aboussekhra, A. and Thoma, F. 1998. Nucleotide excision repair and photolyase preferentially repair the nontranscribed strand of RNA polymerase Ill-transcribed genes in Saccharomyces cerevisiae. Genes Dev 12(3), pp. 411-421.
Alani, E. et al. 1987. A method for gene disruption that allows repeated use of URA3 selection in the construction of multiply disrupted yeast strains. Genetics 116(4), pp. 541-545.
Allinen, M. 2002. DNA damage response genes and chromosome Ilq21-q24 candidate tumor suppressor genes in breast cancer. Thesis, pp. 1-79.
Altaf, M. et al. 2007. Histone modifications in response to DNA damage. Mutat Res 618(1-2), pp. 81-90.
Anderson, J. D. and Widom, J. 2001. Poly(dA-dT) promoter elements increase the equilibrium accessibility o f nucleosomal DNA target sites. Mol Cell Biol 21(11), pp. 3830-3839.
Annunziato, A. T. and Hansen, J. C. 2000. Role of histone acetylation in the assembly and modulation o f chromatin structures. Gene Expr 9(1-2), pp. 37-61.
Aparicio, O. M. et al. 1991. Modifiers of position effect are shared between telomeric and silent mating-type loci in S. cerevisiae. Cell 66(6), pp. 1279-1287.
Aparicio, O. M. and Gottschling, D. E. 1994. Overcoming telomeric silencing: a trans-activator competes to establish gene expression in a cell cycle-dependent way.
Genes Dev 8(10), pp. 1133-1146.
Armstrong, C. M. et al. 2002. Mutations in Saccharomyces cerevisiae gene SIR2 can have differential effects on in vivo silencing phenotypes and in vitro histone deacetylation activity. Mol Biol Cell 13(4), pp. 1427-1438.
Ashktorab, H. et al. 2008. Global Histone H4 Acetylation and HDAC2 Expression in Colon Adenoma and Carcinoma. Dig Dis Sci.
Ataian, Y. and Krebs, J. E. 2006. Five repair pathways in one context: chromatin modification during DNA repair. Biochem Cell Biol 84(4), pp. 490-504.
Auriche, C. et al. 2008. Budding yeast with human telomeres: a puzzling structure.
Biochimie 90(1), pp. 108-115.
Avvakumov, N. and Cote, J. 2007. The MYST family of histone acetyltransferases and their intimate links to cancer. Oncogene 26(37), pp. 5395-5407.
Axelrod, J. D. et al. 1993. GAL4 disrupts a repressing nucleosome during activation of GAL1 transcription in vivo. Genes Dev 7(5), pp. 857-869.
Aylon, Y. and Kupiec, M. 2004. DSB repair: the yeast paradigm. DNA Repair (Amst) 3(8-9), pp. 797-815.
Baer, M. and Sancar, G. B. 1989. Photolyases from Saccharomyces cerevisiae and Escherichia coli recognize common binding determinants in DNA containing pyrimidine dimers. Mol Cell Biol 9(11), pp. 4777-4788.
Bang, D. D. et al. 1992. Molecular cloning of RAD 16, a gene involved in differential repair in Saccharomyces cerevisiae. Nucleic Acids Res 20(15), pp. 3925-3931.
Baudin, A. et al. 1993. A simple and efficient method for direct gene deletion in Saccharomyces cerevisiae. Nucleic Acids Res 21(14), pp. 3329-3330.
Becker, M. M. and Wang, J. C. 1984. Use of light for footprinting DNA in vivo.
Nature 309(5970), pp. 682-687.
Becker, P. B. 2002. Nucleosome sliding: facts and fiction. E M B O J 21(18), pp. 4749- 4753.
Becker, P. B. and Horz, W. 2002. ATP-dependent nucleosome remodeling. Annu Rev
Biochem 71, pp. 247-273.
Bedoyan, J. et al. 1992. Transcription, nucleosome stability, and DNA repair in a yeast minichromosome. J Biol Chem 267(9), pp. 5996-6005.
Bell, S. D. et al. 2002. The interaction of Alba, a conserved archaeal chromatin protein, with Sir2 and its regulation by acetylation. Science 296(5565), pp. 148-151. Benbow, S. Z. and Dubois, M. L. 2008. The dosage o f chromatin proteins affects transcriptional silencing and DNA repair in Saccharomyces cerevisiae. FEBS Lett 582(4), pp. 497-502.
Bennett, R. A. et al. 1997. Interaction of human apurinic endonuclease and DNA polymerase beta in the base excision repair pathway. Proc Natl Acad Sci U S A 94(14), pp. 7166-7169.
Berger, S. L. 2007. The complex language o f chromatin regulation during transcription. Nature 447(7143), pp. 407-412.
Bert, A. G. et al. 2007. A modular enhancer is differentially regulated by GATA and NFAT elements that direct different tissue-specific patterns of nucleosome positioning and inducible chromatin remodeling. Mol Cell Biol 27(8), pp. 2870-2885. Bi, X. et al. 1999. The yeast HML I silencer defines a heterochromatin domain boundary by directional establishment o f silencing. Proc Natl Acad Sci U S A 96(21), pp. 11934-11939.
Bi, X. et al. 2004. Regulation of transcriptional silencing in yeast by growth temperature. J Mol Biol 344(4), pp. 893-905.
Biddick, R. and Young, E. T. 2009. The disorderly study o f ordered recruitment.
Yeast 26(4), pp. 205-220.
Bilaud, T. et al. 1997. Telomeric localization of TRF2, a novel human telobox protein. Nat Genet 17(2), pp. 236-239.
Blander, G. and Guarente, L. 2004. The Sir2 family of protein deacetylases. Annu Rev
Biochem 73, pp. 417-435.
Boeke, J. D. et al. 1984. A positive selection for mutants lacking orotidine-5'- phosphate decarboxylase activity in yeast: 5-fluoro-orotic acid resistance. Mol Gen
Genet 197(2), pp. 345-346.
Boeke, J. D. et al. 1987. 5-Fluoroorotic acid as a selective agent in yeast molecular genetics. Methods Enzymol 154, pp. 164-175.
Boorstein, R. J. et al. 1990. Formation and stability of repairable pyrimidine photohydrates in DNA. Biochemistry 29(46), pp. 10455-10460.
Borra, M. T. et al. 2004. Substrate specificity and kinetic mechanism of the Sir2 family o f NAD+-dependent histone/protein deacetylases. Biochemistry 43(30), pp. 9877-9887.
Boscheron, C. et al. 1996. Cooperation at a distance between silencers and proto silencers at the yeast HML locus. Embo J 15(9), pp. 2184-2195.
Bourgeois, C. A. et al. 1985. New data on the in-situ position of the inactive X chromosome in the interphase nucleus of human fibroblasts. Hum Genet 69(2), pp. 122-129.
Brachmann, C. B. et al. 1995. The SIR2 gene family, conserved from bacteria to humans, functions in silencing, cell cycle progression, and chromosome stability.
Genes Dev 9(23), pp. 2888-2902.
Braunstein, M. et al. 1993. Transcriptional silencing in yeast is associated with reduced nucleosome acetylation. Genes Dev 7(4), pp. 592-604.
Braunstein, M. et al. 1996. Efficient transcriptional silencing in Saccharomyces cerevisiae requires a heterochromatin histone acetylation pattern. Mol Cell Biol 16(8), pp. 4349-4356.
Brownell, J. E. and Allis, C. D. 1996. Special HATs for special occasions: linking histone acetylation to chromatin assembly and gene activation. Curr Opin Genet Dev 6(2), pp. 176-184.
Bryk, M. et al. 1997. Transcriptional silencing o f Tyl elements in the RDN1 locus of yeast. Genes Dev 11(2), pp. 255-269.
Buchman, A. R. et al. 1988. Two DNA-binding factors recognize specific sequences at silencers, upstream activating sequences, autonomously replicating sequences, and telomeres in Saccharomyces cerevisiae. Mol Cell Biol 8(1), pp. 210-225.
Buck, S. W. and Shore, D. 1995. Action of a RAP1 carboxy-terminal silencing domain reveals an underlying competition between HMR and telomeres in yeast.
Genes Dev 9(3), pp. 370-384.
Bugreev, D. V. et al. 2006. Rad54 protein promotes branch migration of Holliday junctions. Nature 442(7102), pp. 590-593.
Caims, B. R. 2005. Chromatin remodeling complexes: strength in diversity, precision through specialization. Curr Opin Genet Dev 15(2), pp. 185-190.
Capiaghi, C. et al. 2004. Kinetochores prevent repair of UV damage in Saccharomyces cerevisiae centromeres. Mol Cell Biol 24(16), pp. 6907-6918.
Carell, T. et al. 2001. The mechanism of action of DNA photolyases. Curr Opin
Chem Biol 5(5), pp. 491-498.
Cavalli, G. and Thoma, F. 1993. Chromatin transitions during activation and repression o f galactose-regulated genes in yeast. E M B O J 12(12), pp. 4603-4613. Chan, C. S. and Tye, B. K. 1983. Organization of DNA sequences and replication origins at yeast telomeres. Cell 33(2), pp. 563-573.
Chaudhuri, S. et al. 2009. Histone H3 Lys79 methylation is required for efficient nucleotide excision repair in a silenced locus of Saccharomyces cerevisiae. Nucleic
Acids Res.
Chen, L. and Widom, J. 2005. Mechanism of transcriptional silencing in yeast. Cell 120(1), pp. 37-48.
Chiani, F. et al. 2006. SIR2 modifies histone H4-K16 acetylation and affects superhelicity in the ARS region of plasmid chromatin in Saccharomyces cerevisiae.
Nucleic Acids Res 34(19), pp. 5426-5437.
Chong, L. et al. 1995. A human telomeric protein. Science 270(5242), pp. 1663-1667. Cline, S. D. and Hanawalt, P. C. 2003. Who's on first in the cellular response to DNA damage? Nat Rev Mol Cell Biol 4(5), pp. 361-372.
Cockell, M. et al. 1995. The carboxy termini of Sir4 and Rapl affect Sir3 localization: evidence for a multicomponent complex required for yeast telomeric silencing. J Cell
Biol 129(4), pp. 909-924.
Coin, F. et al. 2008. Nucleotide excision repair driven by the dissociation of CAK from TFIIH. Mol Cell 31(1), pp. 9-20.
Constantinou, A. et al. 2000. Werner's syndrome protein (WRN) migrates Holliday junctions and co-localizes with RPA upon replication arrest. EMBO Rep 1(1), pp. 80-
84.
Cooke, M. S. et al. 2003. Oxidative DNA damage: mechanisms, mutation, and disease. FASEB J 17(10), pp. 1195-1214.
Dammann, R. et al. 1993. Chromatin structures and transcription o f rDNA in yeast Saccharomyces cerevisiae. Nucleic Acids Res 21(10), pp. 2331-2338.
David, S. S. et al. 2007. Base-excision repair of oxidative DNA damage. Nature 447(7147), pp. 941-950.
de Boer, J. and Hoeijmakers, J. H. 2000. Nucleotide excision repair and human syndromes. Carcinogenesis 21(3), pp. 453-460.
de Bruin, D. et al. 2000. Telomere folding is required for the stable maintenance of telomere position effects in yeast. Mol Cell Biol 20(21), pp. 7991-8000.
de Laat, W. L. et al. 1999. Molecular mechanism of nucleotide excision repair. Genes
Dev 13(7), pp. 768-785.
Deckert, J. and Struhl, K. 2002. Targeted recruitment of Rpd3 histone deacetylase represses transcription by inhibiting recruitment of Swi/Snf, SAGA, and TATA binding protein. Mol Cell Biol 22(18), pp. 6458-6470.
Demple, B. and Linn, S. 1982. 5,6-Saturated thymine lesions in DNA: production by ultraviolet light or hydrogen peroxide. Nucleic Acids Res 10(12), pp. 3781-3789. Demple, B. and Sung, J. S. 2005. Molecular and biological roles of Apel protein in mammalian base excision repair. DNA Repair (Amst) 4(12), pp. 1442-1449.
Dhillon, N. and Kamakaka, R. T. 2000. A histone variant, Htzlp, and a Sirlp-like protein, Esc2p, mediate silencing at HMR. Mol Cell 6(4), pp. 769-780.
Dizdaroglu, M. 2005. Base-excision repair of oxidative DNA damage by DNA glycosylases. Mutat Res 591(1-2), pp. 45-59.
Downs, J. A. et al. 2003. Suppression o f homologous recombination by the Saccharomyces cerevisiae linker histone. Mol Cell 11(6), pp. 1685-1692.
Downs, J. A. et al. 2007. Chromatin dynamics and the preservation of genetic information. Nature 447(7147), pp. 951-958.
Dror, V. and Winston, F. 2004. The Swi/Snf chromatin remodeling complex is required for ribosomal DNA and telomeric silencing in Saccharomyces cerevisiae.
Mol Cell Biol 24(18), pp. 8227-8235.
Dzantiev, L. et al. 2004. A defined human system that supports bidirectional mismatch-provoked excision. Mol Cell 15(1), pp. 31-41.
Ehrenhofer-Murray, A. E. 2004. Chromatin dynamics at DNA replication, transcription and repair. EurJBiochem 271(12), pp. 2335-2349.
Ferreiro, J. A. et al. 2004. Cbflp modulates chromatin structure, transcription and repair at the Saccharomyces cerevisiae MET16 locus. Nucleic Acids Res 32(5), pp.
1617-1626.
Field, Y. et al. 2008. Distinct modes of regulation by chromatin encoded through nucleosome positioning signals. PLoS ComputBiol 4(11), p. el000216.
Fillingham, J. et al. 2008. Chaperone control of the activity and specificity of the histone H3 acetyltransferase Rttl09. Mol Cell Biol 28(13), pp. 4342-4353.
Fisher, T. S. and Zakian, V. A. 2005. Ku: a multifunctional protein involved in telomere maintenance. DNA Repair (Amst) 4(11), pp. 1215-1226.
Flynn, P. J. and Reece, R. J. 1999. Activation of transcription by metabolic intermediates o f the pyrimidine biosynthetic pathway. Mol Cell Biol 19(1), pp. 882-
8 8 8.
Francois, F. et al. 2004. Development of an integrative transformation system for the opportunistic pathogenic yeast Candida lusitaniae using URA3 as a selection marker.
Yeast 21(2), pp. 95-106.
Freeman-Cook, L. L. et al. 2005. Conserved locus-specific silencing functions of Schizosaccharomyces pombe sir2+. Genetics 169(3), pp. 1243-1260.
Friedberg, E. C. 1996. Relationships between DNA repair and transcription. Annu Rev
Biochem 65, pp. 15-42.
Friedberg, E. C. 2003. DNA damage and repair. Nature 421(6921), pp. 436-440. Friedberg, E. C. et al. 2005. DNA repair and mutagenesis. 2nd ed. Washington DC: ASM Press.
Fritze, C. E. et al. 1997. Direct evidence for SIR2 modulation of chromatin structure in yeast rDNA. Embo J 16(21), pp. 6495-6509.
Fukuda, H. et al. 2006. Simple histone acetylation plays a complex role in the regulation o f gene expression. Brief Funct Genomic Proteomic 5(3), pp. 190-208. Galvao, T. C. and de Lorenzo, V. 2005. Adaptation of the yeast URA3 selection system to gram-negative bacteria and generation of a {deltajbetCDE Pseudomonas putida strain. Appl Environ Microbiol 71(2), pp. 883-892.
Gao, L. and Gross, D. S. 2006. Using genomics and proteomics to investigate mechanisms of transcriptional silencing in Saccharomyces cerevisiae. Brief Funct
Gao, L. and Gross, D. S. 2008. Sir2 silences gene transcription by targeting the transition between RNA polymerase II initiation and elongation. Mol Cell Biol 28(12), pp. 3979-3994.
Gardner, K. A. and Fox, C. A. 2001. The Sirl protein's association with a silenced chromosome domain. Genes Dev 15(2), pp. 147-157.
Gasser, S. M. and Cockell, M. M. 2001. The molecular biology of the SIR proteins.
Gene 279(1), pp. 1-16.
Georgel, P. T. and Hansen, J. C. 2001. Linker histone function in chromatin: dual mechanisms o f action. Biochem Cell Biol 79(3), pp. 313-316.
Geraghty, D. S. et al. 1998. Evidence that partial unwrapping of DNA from nucleosomes facilitates the binding of heat shock factor following DNA replication in yeast. J Biol Chem 273(32), pp. 20463-20472.
Ghidelli, S. et al. 2001. Sir2p exists in two nucleosome-binding complexes with distinct deacetylase activities. E m b o J 20(16), pp. 4522-4535.
Gietz, D. et al. 1992. Improved method for high efficiency transformation of intact yeast cells. Nucleic Acids Res 20(6), p. 1425.
Gong, F. et al. 2006. Rad4-Rad23 interaction with SWI/SNF links ATP-dependent chromatin remodeling with nucleotide excision repair. Nat Struct Mol Biol 13(10), pp. 902-907.
Gong, F. et al. 2005. Nucleotide excision repair in chromatin and the right of entry.
DNA Repair (Amst) 4(8), pp. 884-896.
Gordon, L. K. and Haseltine, W. A. 1982. Quantitation of cyclobutane pyrimidine dimer formation in double- and single-stranded DNA fragments of defined sequence.
Radiat Res 89(1), pp. 99-112.
Gotta, M. et al. 1997. Localization of Sir2p: the nucleolus as a compartment for silent information regulators. E M B O J 16(11), pp. 3243-3255.
Gottschling, D. E. 1992. Telomere-proximal DNA in Saccharomyces cerevisiae is refractory to methyltransferase activity in vivo. Proc Natl Acad Sci U S A 89(9), pp. 4062-4065.
Gottschling, D. E. et al. 1990. Position effect at S. cerevisiae telomeres: reversible repression o f Pol II transcription. Cell 63(4), pp. 751-762.
Grandin, N. et al. 2001. Tenl functions in telomere end protection and length regulation in association with Stnl and Cdcl3. EM B O J 20(5), pp. 1173-1183.
Grandin, N. et al. 1997. Stnl, a new Saccharomyces cerevisiae protein, is implicated in telomere size regulation in association with Cdcl3. Genes Dev 11(4), pp. 512-527.
Grant, P. A. and Berger, S. L. 1999. Histone acetyltransferase complexes. Semin Cell
Dev Biol 10(2), pp. 169-177.
Grant, P. A. et al. 1997. Yeast Gcn5 functions in two multisubunit complexes to acetylate nucleosomal histones: characterization of an Ada complex and the SAGA (Spt/Ada) complex. Genes Dev 11(13), pp. 1640-1650.
Green, C. M. and Almouzni, G. 2002. When repair meets chromatin. First in series on chromatin dynamics. EMBO Rep 3(1), pp. 28-33.
Gregoire, S. and Yang, X. J. 2005. Association with class Ha histone deacetylases upregulates the sumoylation of MEF2 transcription factors. Mol Cell Biol 25(6), pp. 2273-2287.
Grossi, S. et al. 2001. Telomere formation by raplp binding site arrays reveals end- specific length regulation requirements and active telomeric recombination. Mol Cell
Biol 21(23), pp. 8117-8128.
Grummt, I. and Pikaard, C. S. 2003. Epigenetic silencing of RNA polymerase I transcription. Nat Rev M ol Cell Biol 4(8), pp. 641-649.
Gueldener, U. et al. 2002. A second set of loxP marker cassettes for Cre-mediated multiple gene knockouts in budding yeast. Nucleic Acids Res 30(6), p. e23.
Guldener, U. et al. 1996. A new efficient gene disruption cassette for repeated use in budding yeast. Nucleic Acids Res 24(13), pp. 2519-2524.
Guzder, S. N. et al. 1995. Reconstitution of yeast nucleotide excision repair with purified Rad proteins, replication protein A, and transcription factor TFIIH. J Biol
Chem 270(22), pp. 12973-12976.
Guzder, S. N. et al. 2006. Complex formation with damage recognition protein Rad 14 is essential for Saccharomyces cerevisiae Radi-Rad 10 nuclease to perform its function in nucleotide excision repair in vivo. Mol Cell Biol 26(3), pp. 1135-1141. Guzder, S. N. et al. 1999. Synergistic interaction between yeast nucleotide excision repair factors NEF2 and NEF4 in the binding of ultraviolet-damaged DNA. J Biol
Chem 274(34), pp. 24257-24262.
Haber, J. E. 1998. Mating-type gene switching in Saccharomyces cerevisiae. Annu
Rev Genet 32, pp. 561-599.
Haidar, D. and Kamakaka, R. T. 2008. Schizosaccharomyces pombe Hst4 functions in DNA damage response by regulating histone H3 K56 acetylation. Eukaryot Cell 7(5), pp. 800-813.
Hara, R. and Sancar, A. 2002. The SWI/SNF chromatin-remodeling factor stimulates repair by human excision nuclease in the mononucleosome core particle. Mol Cell
Hardy, C. F. et al. 1992. A RAP 1-interacting protein involved in transcriptional silencing and telomere length regulation. Genes Dev 6(5), pp. 801-814.
Hecht, A. et al. 1995. Histone H3 and H4 N-termini interact with SIR3 and SIR4 proteins: a molecular model for the formation of heterochromatin in yeast. Cell 80(4), pp. 583-592.
Hefferin, M. L. and Tomkinson, A. E. 2005. Mechanism of DNA double-strand break repair by non-homologous end joining. DNA Repair (Amst) 4(6), pp. 639-648.
Hendrickson, E. A. 1997. Cell-cycle regulation of mammalian DNA double-strand- break repair. Am J Hum Genet 61(4), pp. 795-800.
Herrero, E. et al. 2008. Redox control and oxidative stress in yeast cells. Biochim
Biophys Acta 1780(11), pp. 1217-1235.
Hickman, M. et al. 2007. Isolation and characterization of conditional alleles of the yeast SIR2 gene. J Mol Biol 367(5), pp. 1246-1257.
Hitomi, K. et al. 1997. Binding and catalytic properties of Xenopus (6-4) photolyase.
J B io l Chem 272(51), pp. 32591-32598.