The Histone Chaperone Asf1 Increases the Rate of Histone Eviction at the Yeast PHO5 and PHO8 Promoters

Eukaryotic gene expression starts off from a largely obstructive chromatin substrate that has to be rendered accessible by regulated mechanisms of chromatin remodeling. The yeast PHO5 promoter is a well known example for the contribution of positioned nucleosomes to gene repression and for extensive chromatin remodeling in the course of gene induction. Recently, the mechanism of this remodeling process was shown to lead to the disassembly of promoter nucleosomes and the eviction of the constituent histones in trans. This finding called for a histone acceptor in trans and thus made histone chaperones likely to be involved in this process. In this study we have shown that the histone chaperone Asf1 increases the rate of histone eviction at the PHO5 promoter. In the absence of Asf1 histone eviction is delayed, but the final outcome of the chromatin transition is not affected. The same is true for the coregulated PHO8 promoter where induction also leads to histone eviction and where the rate of histone loss is reduced in asf1 strains as well, although less severely. Importantly, the final extent of chromatin remodeling is not affected. We have also presented evidence that Asf1 and the SWI/SNF chromatin remodeling complex work in distinct parallel but functionally overlapping pathways, i.e. they both contribute toward the same outcome without being mutually strictly dependent. Eukaryotic gene expression starts off from a largely obstructive chromatin substrate that has to be rendered accessible by regulated mechanisms of chromatin remodeling. The yeast PHO5 promoter is a well known example for the contribution of positioned nucleosomes to gene repression and for extensive chromatin remodeling in the course of gene induction. Recently, the mechanism of this remodeling process was shown to lead to the disassembly of promoter nucleosomes and the eviction of the constituent histones in trans. This finding called for a histone acceptor in trans and thus made histone chaperones likely to be involved in this process. In this study we have shown that the histone chaperone Asf1 increases the rate of histone eviction at the PHO5 promoter. In the absence of Asf1 histone eviction is delayed, but the final outcome of the chromatin transition is not affected. The same is true for the coregulated PHO8 promoter where induction also leads to histone eviction and where the rate of histone loss is reduced in asf1 strains as well, although less severely. Importantly, the final extent of chromatin remodeling is not affected. We have also presented evidence that Asf1 and the SWI/SNF chromatin remodeling complex work in distinct parallel but functionally overlapping pathways, i.e. they both contribute toward the same outcome without being mutually strictly dependent. The DNA of eukaryotic cells is compacted in the nucleus into a complex structure called chromatin. The first level of chromatin organization is formed by the nucleosome, which consists of a histone octamer core organizing ∼1.7 turns of double-stranded DNA around its surface (1Luger K. Mader A.W. Richmond R.K. Sargent D.F. Richmond T.J. Nature. 1997; 389: 251-260Crossref PubMed Scopus (6725) Google Scholar). DNA that is wound around a histone octamer in a canonical nucleosome is much less accessible for most DNA-interacting factors than DNA in the linker regions between nucleosomes. It is now widely accepted not only that nucleosomes serve a structural role for the compaction of eukaryotic DNA but also that the obstructive nature of the nucleosomal histone-DNA interactions is a means to regulate the expression of genetic information (2Roeder R.G. FEBS Lett. 2005; 579: 909-915Crossref PubMed Scopus (255) Google Scholar, 3Fyodorov D.V. Kadonaga J.T. Cell. 2001; 106: 523-525Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar, 4Narlikar G.J. Fan H.Y. Kingston R.E. Cell. 2002; 108: 475-487Abstract Full Text Full Text PDF PubMed Scopus (1228) Google Scholar). This mode of regulation involves changes in chromatin structure at, for example, promoter or enhancer regions. A hallmark of such regulatory changes is the switch of DNA regions from a state that is protected from nucleases to a state that is sensitive, or even hypersensitive, to nucleases. To understand the process of regulation through chromatin structure it is therefore crucial to study the molecular mechanisms that lead to the inducible generation of hypersensitive sites. To this end, the PHO5 promoter in yeast became a classical model system (5Svaren J. Hörz W. Trends Biochem. Sci. 1997; 22: 93-97Abstract Full Text PDF PubMed Scopus (155) Google Scholar). In its repressed state this promoter region is organized into four positioned nucleosomes with a short hypersensitive site in the middle. Upon activation by phosphate starvation this characteristic chromatin organization becomes remodeled into an extended hypersensitive region (6Almer A. Rudolph H. Hinnen A. Hörz W. EMBO J. 1986; 5: 2689-2696Crossref PubMed Scopus (347) Google Scholar). The promoter nucleosomes in this induced state are completely disassembled as assayed by the loss of histone DNA contacts (7Reinke H. Hörz W. Mol. Cell. 2003; 11: 1599-1607Abstract Full Text Full Text PDF PubMed Scopus (332) Google Scholar, 8Reinke H. Hörz W. Biochim. Biophys. Acta. 2004; 1677: 24-29Crossref PubMed Scopus (32) Google Scholar, 9Boeger H. Griesenbeck J. Strattan J.S. Kornberg R.D. Mol. Cell. 2003; 11: 1587-1598Abstract Full Text Full Text PDF PubMed Scopus (331) Google Scholar). Recently, we and others showed that this loss of nucleosomal organization corresponds to a movement of histones away from the promoter in trans (10Korber P. Luckenbach T. Blaschke D. Hörz W. Mol. Cell. Biol. 2004; 24: 10965-10974Crossref PubMed Scopus (76) Google Scholar, 11Boeger H. Griesenbeck J. Strattan J.S. Kornberg R.D. Mol. Cell. 2004; 14: 667-673Abstract Full Text Full Text PDF PubMed Scopus (200) Google Scholar), raising the mechanistic question of where the histones go. Free histones together with DNA are notoriously aggregation prone, and it is assumed that they occur in the cell mainly in complex with nucleic acids or histone chaperones (12Verreault A. Genes Dev. 2000; 14: 1430-1438PubMed Google Scholar, 13Tyler J.K. Eur. J. Biochem. 2002; 269: 2268-2274Crossref PubMed Scopus (123) Google Scholar, 14Loyola A. Almouzni G. Biochim. Biophys. Acta. 2004; 1677: 3-11Crossref PubMed Scopus (272) Google Scholar). Histone chaperones are a diverse family of proteins that interact with various kinds of histones and probably serve mainly as histone donors and acceptors during nucleosome assembly or disassembly processes. In addition, they can have regulatory functions as in the case of the Hir proteins or Asf1 (15Osley M.A. Lycan D. Mol. Cell. Biol. 1987; 7: 4204-4210Crossref PubMed Scopus (90) Google Scholar, 16Sutton A. Bucaria J. Osley M.A. Sternglanz R. Genetics. 2001; 158: 587-596Crossref PubMed Google Scholar). Histone chaperones appear to form a redundant network as yeast strains deleted in multiple histone chaperone genes are viable (13Tyler J.K. Eur. J. Biochem. 2002; 269: 2268-2274Crossref PubMed Scopus (123) Google Scholar). Nonetheless, histone chaperones can also be specific for certain histone variants (17Tagami H. Ray-Gallet D. Almouzni G. Nakatani Y. Cell. 2004; 116: 51-61Abstract Full Text Full Text PDF PubMed Scopus (960) Google Scholar) or for certain processes, e.g. for replication-dependent or -independent chromatin assembly (18Ray-Gallet D. Almouzni G. Methods Enzymol. 2004; 375: 117-131Crossref PubMed Scopus (14) Google Scholar, 19Ray-Gallet D. Quivy J.P. Scamps C. Martini E.M. Lipinski M. Almouzni G. Mol. Cell. 2002; 9: 1091-1100Abstract Full Text Full Text PDF PubMed Scopus (303) Google Scholar). Chromatin remodeling complexes may work more or less specifically with, or may even contain, histone chaperones (14Loyola A. Almouzni G. Biochim. Biophys. Acta. 2004; 1677: 3-11Crossref PubMed Scopus (272) Google Scholar, 20Ito T. Bulger M. Kobayashi R. Kadonaga J.T. Mol. Cell. Biol. 1996; 16: 3112-3124Crossref PubMed Scopus (227) Google Scholar, 21Shen X. Ranallo R. Choi E. Wu C. Mol. Cell. 2003; 12: Full Text Full Text PDF PubMed Scopus Google Scholar, G. X. J. Wu Wu C. 2004; PubMed Scopus Google Scholar, A. G. D. Genes Dev. 2001; Google Scholar). histone chaperones are likely for the histone acceptor in the process of histone eviction in trans remodeling of PHO5 promoter chromatin. In this study we the of in genes for various histone chaperones the induction of the PHO5 histone only the of Asf1 showed an PHO5 induction. The rate of chromatin remodeling was delayed, the final extent of chromatin remodeling and gene expression was not We also extended study to the PHO8 gene that for an and is coregulated with PHO5 by the same M. Hörz W. J. Biol. 2000; Full Text Full Text PDF PubMed Scopus Google Scholar, Hörz W. 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Mol. Cell. Biol. 2005; PubMed Scopus Google Scholar, Mol. Cell. Biol. 2003; PubMed Scopus Google Scholar). We also this for the histone chaperone strains by induction The deleted in the gene showed a in PHO5 induction was in deleted for and not The also showed a in PHO5 induction. by during induction we that the in induction was not of the level of chromatin not as was by J.K. Mol. Cell. 2004; 14: Full Text Full Text PDF PubMed Scopus Google Scholar) in during induction of a the induction of in the was more than in but not a the level of chromatin as with the asf1 not not PHO5 induction not and we the role of The of Asf1 the of PHO5 the of Chromatin the of the asf1 as the level of PHO5 was of a at the chromatin transition The course of chromatin remodeling at the PHO5 promoter during induction in asf1 and strains was by the of the site in the PHO5 promoter region (6Almer A. Rudolph H. Hinnen A. Hörz W. EMBO J. 1986; 5: 2689-2696Crossref PubMed Scopus (347) Google Scholar, Hörz W. Methods Mol. Biol. Google Scholar). A in nucleosome remodeling was In addition, we the loss of histones from the PHO5 promoter region by with the of histone in the or with the of histone in the not The was for region as to an of PHO5 not changes in histone (7Reinke H. Hörz W. Mol. Cell. 2003; 11: 1599-1607Abstract Full Text Full Text PDF PubMed Scopus (332) Google Scholar). This chromatin also showed a for the asf1 in both but in between the and asf1 strains was both chromatin that the rate of chromatin than only in the gene expression is in the absence of It was shown that of to its site chromatin J. J. A. Hörz W. EMBO J. PubMed Scopus Google Scholar). We therefore that the in chromatin remodeling also a in to the promoter. by we in asf1 strains that to the promoter was as chromatin remodeling in a not The in asf1 to of the Chromatin we of the PHO5 promoter in which both are by to for that a have of the chromatin remodeling at the PHO5 promoter J. A. Hörz W. EMBO J. 2001; PubMed Scopus Google Scholar, A. M. Hörz W. Mol. Cell. Full Text Full Text PDF PubMed Scopus Google Scholar). In such a the same chromatin transition and promoter activation induction as with the promoter phosphate starvation G. The of for of the Chromatin at the in Scholar). that is to the chromatin remodeling also the chromatin transition in this The induction of the promoter through the was in an asf1 as the induction of the promoter through the This was not of the or as the induction of the promoter was by the asf1 The asf1 even showed a much extent of final induction for the than the not We that asf1 strains to final than the strains for and induced of PHO5 induction or for final such expression are not with changes in the chromatin structure not and are probably to gene The of the and Genes a the of chromatin has that is for PHO5 promoter chromatin. the absence of leads to a in PHO5 (7Reinke H. Hörz W. Mol. 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PubMed Scopus Google Scholar). of induction less accessible in asf1 than in cells Nonetheless, we in by site that remodeling in asf1 even of induction in induction In addition, the induction of an in phosphate to the same chromatin the of the asf1 induction was from the was the case for the PHO5 at the PHO8 promoter the level of chromatin was with the or histone chaperone strains not that the rate of chromatin remodeling at the PHO8 promoter was in the absence of although not as as at the PHO5 promoter and and and and that remodeling was Asf1 for PHO5 J.K. Mol. Cell. 2004; 14: Full Text Full Text PDF PubMed Scopus Google Scholar) that Asf1 is for PHO5 and PHO8 we have shown that induction of both was in asf1 for and it is known that the phosphate M. P. M. EMBO J. 7: PubMed Scopus Google Scholar) phosphate that of in to the phosphate in the between the from and the be to the induction and A. Mol. Cell. Biol. 2005; PubMed Scopus Google Scholar) showed that the and which are not for PHO5 induction and chromatin (7Reinke H. Hörz W. Mol. Cell. 2003; 11: 1599-1607Abstract Full Text Full Text PDF PubMed Scopus (332) Google Scholar, J. A. Hörz W. EMBO J. 2001; PubMed Scopus Google Scholar, A. Mol. Cell. Biol. 2005; PubMed Scopus Google Scholar, Mol. Cell. Biol. 2003; PubMed Scopus Google Scholar), The induction by various of phosphate in the induction We the same to the Asf1 for PHO5 induction at various phosphate the phosphate the induction of PHO5 was more in the asf1 than in the cells certain of phosphate the induction of the asf1 was induction of the In this study we have shown that the histone chaperone Asf1 increases the rate of histone eviction during induction of the yeast PHO5 and PHO8 both the of chromatin remodeling and induction in asf1 a is of with PHO5 induction in strains deleted in the genes for the histone or the also lead to a in PHO5 induction the chromatin (7Reinke H. Hörz W. Mol. Cell. 2003; 11: 1599-1607Abstract Full Text Full Text PDF PubMed Scopus (332) Google Scholar, J. A. Hörz W. EMBO J. 2001; PubMed Scopus Google Scholar, A. Mol. Cell. Biol. 2005; PubMed Scopus Google Scholar, Mol. Cell. Biol. 2003; PubMed Scopus Google Scholar). in the case of the coregulated PHO8 promoter that is and A. M. M. Hörz W. EMBO J. PubMed Scopus Google Scholar) a are known The asf1 is the first of this Importantly, induction of the asf1 i.e. in the absence of to the extent of and the final as or even than in is an for chromatin remodeling at the PHO5 and PHO8 This is not as histone chaperones a notoriously redundant system in yeast (13Tyler J.K. Eur. J. Biochem. 2002; 269: 2268-2274Crossref PubMed Scopus (123) Google Scholar). the mechanism of chromatin remodeling at both in the to have of for Asf1 as the absence of four histone i.e. or not A role for a histone chaperone in remodeling of PHO5 promoter chromatin with the that a remodeling mechanism to histone eviction in trans (10Korber P. Luckenbach T. Blaschke D. Hörz W. Mol. Cell. Biol. 2004; 24: 10965-10974Crossref PubMed Scopus (76) Google Scholar, 11Boeger H. Griesenbeck J. Strattan J.S. Kornberg R.D. Mol. Cell. 2004; 14: 667-673Abstract Full Text Full Text PDF PubMed Scopus (200) Google Scholar) in or a histone acceptor in trans as of histone chaperones be less likely histones to the promoter region by a mechanism in In we this to that the contribution of the histone chaperone Asf1 to PHO8 promoter chromatin remodeling for a mechanism of histone eviction in trans at this promoter as induction of the promoter was also shown to lead to the of histones Y. 2004; PubMed Scopus Google Scholar, M.A. K. Mol. Cell. Biol. 2004; 24: PubMed Scopus Google Scholar), but we have shown that Asf1 not the rate of induction of the coregulated promoter. This may that histone eviction at the not occur a trans or that is a for a histone It that Asf1 not have a role in activation in Recently, study also the role of Asf1 in the induction of PHO5 and PHO8 J.K. Mol. Cell. 2004; 14: Full Text Full Text PDF PubMed Scopus Google Scholar). The to the that the PHO5 the coregulated PHO8 gene be induced in asf1 strains at and therefore Asf1 as for activation of are in with the that Asf1 a role in chromatin remodeling and the activation of both but we have shown that chromatin remodeling at both genes can be to in the absence of The between the can be by in the induction It is that the extent of induction of the can be by the phosphate in the and that of lead to more of the PHO5 gene for example, or A. Mol. Cell. Biol. 2005; PubMed Scopus Google Scholar). We the induction of PHO5 in an asf1 and at various of phosphate in the induction induction in which a is induced an asf1 is J.K. Mol. Cell. 2004; 14: Full Text Full Text PDF PubMed Scopus Google Scholar) made of induction that is by a M. P. M. EMBO J. 7: PubMed Scopus Google Scholar). In to such of phosphate and may even but cell such probably corresponds to as and by A. Mol. Cell. Biol. 2005; PubMed Scopus Google Scholar, M. 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Biol. 2003; PubMed Scopus Google Scholar). we have evidence that the SWI/SNF complex can work together with the histone chaperone that the SWI/SNF complex is an example of a chromatin that can histone eviction in trans in that the role of Asf1 in nucleosome eviction is not with the remodeling of the SWI/SNF i.e. that the SWI/SNF complex and the histone chaperone Asf1 work in distinct parallel that functionally The SWI/SNF complex and Asf1 can with histone chaperones or The is as Chromatin remodeling at the PHO8 promoter has to a This is in asf1 that Asf1 to the outcome of this but can be by chromatin remodeling at the PHO5 promoter involves a as well but can also be in the absence of through at a This in can also with as a of Asf1 in a leads to a with even induction and even state induction during induction the in phosphate we be the of or histone chaperones at the in case to the same final outcome of remodeled chromatin that the of the e.g. histone eviction in trans through the of a chromatin and a histone are We and for strains and for We for of the