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Article ; Online: A screen for histone mutations that affect quiescence in S. cerevisiae.

Small, Eric M / Osley, Mary Ann

2023 Volume 290, Issue 14, Page(s) 3539–3562

Abstract: Quiescence or G0 is a reversible state in which cells cease division but retain the ability to resume proliferation. Quiescence occurs in all organisms and is essential for stem cell maintenance and tissue renewal. It is also related to chronological ... ...

Abstract	Quiescence or G0 is a reversible state in which cells cease division but retain the ability to resume proliferation. Quiescence occurs in all organisms and is essential for stem cell maintenance and tissue renewal. It is also related to chronological lifespan (CLS)-the survival of postmitotic quiescent cells (Q cells) over time-and thus contributes to longevity. Important questions remain regarding the mechanisms that control entry into quiescence, maintenance of quiescence and re-entry of Q cells into the cell cycle. S. cerevisiae has emerged as an excellent organism in which to address these questions because of the ease in which Q cells can be isolated. Following entry into G0, yeast cells remain viable for an extended period and can re-enter the cell cycle when exposed to growth-promoting signals. Histone acetylation is lost during the formation of Q cells and chromatin becomes highly condensed. This unique chromatin landscape regulates quiescence-specific transcriptional repression and has been linked to the formation and maintenance of Q cells. To ask whether other chromatin features regulate quiescence, we conducted two comprehensive screens of histone H3 and H4 mutants and identified mutants that show either altered quiescence entry or CLS. Examination of several quiescence entry mutants found that none of the mutants retain histone acetylation in Q cells but show differences in chromatin condensation. A comparison of H3 and H4 mutants with altered CLS to those with altered quiescence entry found that chromatin plays both overlapping and independent roles in the continuum of the quiescence program.
MeSH term(s)	Histones/genetics ; Histones/metabolism ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/metabolism ; Cell Division ; Chromatin/genetics ; Chromatin/metabolism ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Mutation
Chemical Substances	Histones ; Chromatin ; Saccharomyces cerevisiae Proteins
Language	English
Publishing date	2023-03-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16759
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Article ; Online: Who gets a license: DNA synthesis in quiescent cells re-entering the cell cycle.

Lee, Po-Hsuen / Osley, Mary Ann

Current genetics

2021 Volume 67, Issue 4, Page(s) 539–543

Abstract: The precise regulation of the entry into S phase is critical for preventing genome instability. The first step in the initiation of eukaryotic DNA synthesis occurs in G1 phase cells and involves the loading of the conserved MCM helicase onto multiple ... ...

Abstract	The precise regulation of the entry into S phase is critical for preventing genome instability. The first step in the initiation of eukaryotic DNA synthesis occurs in G1 phase cells and involves the loading of the conserved MCM helicase onto multiple origins of replication in a process known as origin licensing. In proliferating metazoan cells, an origin-licensing checkpoint delays initiation until high levels of MCM loading occur, with excess origins being licensed. One function of this checkpoint is to ensure that S phase can be completed in the face of replication stress by activation of dormant MCM bound origins. However, when both metazoan and yeast cells enter S phase from quiescence or G0 phase, a non-growing but reversible cell cycle state, origins are significantly under-licensed. In metazoan cells, under-licensing is the result of a compromised origin-licensing checkpoint. In budding yeast, our study has revealed that under-licensing can be attributed to the chromatin structure at a class of origins that is inhibitory to the binding of MCM. Thus, defects in multiple pathways may contribute to the failure to fully license origins in quiescent cells re-entering the cell cycle, thereby promoting a higher risk of genome instability.
MeSH term(s)	Cell Cycle/genetics ; Cell Division/genetics ; Chromatin/genetics ; DNA/biosynthesis ; DNA/genetics ; DNA Replication/genetics ; Genomic Instability/genetics ; Humans ; Replication Origin/genetics ; Saccharomyces cerevisiae/genetics
Chemical Substances	Chromatin ; DNA (9007-49-2)
Language	English
Publishing date	2021-03-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	282876-5
ISSN	1432-0983 ; 0172-8083
ISSN (online)	1432-0983
ISSN	0172-8083
DOI	10.1007/s00294-021-01170-7
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Article ; Online: Chromatin structure restricts origin utilization when quiescent cells re-enter the cell cycle.

Lee, Po-Hsuen / Osley, Mary Ann

Nucleic acids research

2021 Volume 49, Issue 2, Page(s) 864–878

Abstract: Quiescent cells reside in G0 phase, which is characterized by the absence of cell growth and proliferation. These cells remain viable and re-enter the cell cycle when prompted by appropriate signals. Using a budding yeast model of cellular quiescence, we ...

Abstract	Quiescent cells reside in G0 phase, which is characterized by the absence of cell growth and proliferation. These cells remain viable and re-enter the cell cycle when prompted by appropriate signals. Using a budding yeast model of cellular quiescence, we investigated the program that initiated DNA replication when these G0 cells resumed growth. Quiescent cells contained very low levels of replication initiation factors, and their entry into S phase was delayed until these factors were re-synthesized. A longer S phase in these cells correlated with the activation of fewer origins of replication compared to G1 cells. The chromatin structure around inactive origins in G0 cells showed increased H3 occupancy and decreased nucleosome positioning compared to the same origins in G1 cells, inhibiting the origin binding of the Mcm4 subunit of the MCM licensing factor. Thus, quiescent yeast cells are under-licensed during their re-entry into S phase.
MeSH term(s)	Cell Cycle/genetics ; Cell Cycle/physiology ; Cell Cycle Checkpoints ; Chromatin/genetics ; Chromatin/ultrastructure ; Chromatin Assembly and Disassembly ; Chromatin Immunoprecipitation ; DNA Replication ; DNA, Fungal/biosynthesis ; DNA, Fungal/genetics ; Minichromosome Maintenance Complex Component 4/metabolism ; Nucleosomes/metabolism ; Nucleosomes/ultrastructure ; Replication Origin/genetics ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/ultrastructure ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism
Chemical Substances	Chromatin ; DNA, Fungal ; Nucleosomes ; Saccharomyces cerevisiae Proteins ; MCM4 protein, S cerevisiae (EC 3.6.4.12) ; Minichromosome Maintenance Complex Component 4 (EC 3.6.4.12)
Language	English
Publishing date	2021-01-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkaa1148
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Article ; Online: A screen for histone mutations that affect quiescence in S. cerevisiae

Small, Eric M. / Osley, Mary Ann

The FEBS Journal. 2023 July, v. 290, no. 14 p.3539-3562

2023

Abstract	Quiescence or G0 is a reversible state in which cells cease division but retain the ability to resume proliferation. Quiescence occurs in all organisms and is essential for stem cell maintenance and tissue renewal. It is also related to chronological lifespan (CLS)—the survival of postmitotic quiescent cells (Q cells) over time—and thus contributes to longevity. Important questions remain regarding the mechanisms that control entry into quiescence, maintenance of quiescence and re‐entry of Q cells into the cell cycle. S. cerevisiae has emerged as an excellent organism in which to address these questions because of the ease in which Q cells can be isolated. Following entry into G0, yeast cells remain viable for an extended period and can re‐enter the cell cycle when exposed to growth‐promoting signals. Histone acetylation is lost during the formation of Q cells and chromatin becomes highly condensed. This unique chromatin landscape regulates quiescence‐specific transcriptional repression and has been linked to the formation and maintenance of Q cells. To ask whether other chromatin features regulate quiescence, we conducted two comprehensive screens of histone H3 and H4 mutants and identified mutants that show either altered quiescence entry or CLS. Examination of several quiescence entry mutants found that none of the mutants retain histone acetylation in Q cells but show differences in chromatin condensation. A comparison of H3 and H4 mutants with altered CLS to those with altered quiescence entry found that chromatin plays both overlapping and independent roles in the continuum of the quiescence program.
Keywords	acetylation ; cell cycle ; chromatin ; histones ; longevity ; stem cells ; transcription (genetics) ; yeasts
Language	English
Dates of publication	2023-07
Size	p. 3539-3562.
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	JOURNAL ARTICLE
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16759
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Article ; Online: FACT and the H2B N tail.

Osley, Mary Ann

Molecular and cellular biology

2013 Volume 34, Issue 3, Page(s) 300–302

Abstract: The FACT histone chaperone/nucleosome reorganization factor plays key roles in nucleosome dynamics during transcription. A new study has linked a specific domain in the H2B N terminus to the activity of FACT in regulating nucleosome disassembly at ... ...

Abstract	The FACT histone chaperone/nucleosome reorganization factor plays key roles in nucleosome dynamics during transcription. A new study has linked a specific domain in the H2B N terminus to the activity of FACT in regulating nucleosome disassembly at promoters during transcription activation and nucleosome reassembly at coding regions during transcription elongation.
MeSH term(s)	DNA-Binding Proteins/metabolism ; High Mobility Group Proteins/metabolism ; Histones/metabolism ; Humans ; Nucleosomes/metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; Transcriptional Elongation Factors/metabolism
Chemical Substances	DNA-Binding Proteins ; FACT protein, S cerevisiae ; High Mobility Group Proteins ; Histones ; Nucleosomes ; Saccharomyces cerevisiae Proteins ; Transcriptional Elongation Factors
Language	English
Publishing date	2013-11-25
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.01519-13
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Zs.A 1666: Show issues

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Article: Who gets a license: DNA synthesis in quiescent cells re-entering the cell cycle

Lee, Po-Hsuen / Osley, Mary Ann

Current genetics. 2021 Aug., v. 67, no. 4

2021

Abstract	The precise regulation of the entry into S phase is critical for preventing genome instability. The first step in the initiation of eukaryotic DNA synthesis occurs in G1 phase cells and involves the loading of the conserved MCM helicase onto multiple origins of replication in a process known as origin licensing. In proliferating metazoan cells, an origin-licensing checkpoint delays initiation until high levels of MCM loading occur, with excess origins being licensed. One function of this checkpoint is to ensure that S phase can be completed in the face of replication stress by activation of dormant MCM bound origins. However, when both metazoan and yeast cells enter S phase from quiescence or G0 phase, a non-growing but reversible cell cycle state, origins are significantly under-licensed. In metazoan cells, under-licensing is the result of a compromised origin-licensing checkpoint. In budding yeast, our study has revealed that under-licensing can be attributed to the chromatin structure at a class of origins that is inhibitory to the binding of MCM. Thus, defects in multiple pathways may contribute to the failure to fully license origins in quiescent cells re-entering the cell cycle, thereby promoting a higher risk of genome instability.
Keywords	Animalia ; DNA replication ; chromatin ; genetic instability ; interphase ; risk ; yeasts
Language	English
Dates of publication	2021-08
Size	p. 539-543.
Publishing place	Springer Berlin Heidelberg
Document type	Article
Note	Review
ZDB-ID	282876-5
ISSN	1432-0983 ; 0172-8083
ISSN (online)	1432-0983
ISSN	0172-8083
DOI	10.1007/s00294-021-01170-7
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Article ; Online: Introduction. Histone ubiquitylation.

Osley, Mary Ann

Methods (San Diego, Calif.)

2011 Volume 54, Issue 3, Page(s) 295

MeSH term(s)	Analytic Sample Preparation Methods ; Cell-Free System ; Chromatin/metabolism ; Histones/metabolism ; Humans ; Transcription, Genetic ; Ubiquitination
Chemical Substances	Chromatin ; Histones
Language	English
Publishing date	2011-07
Publishing country	United States
Document type	Introductory Journal Article
ZDB-ID	1066584-5
ISSN	1095-9130 ; 1046-2023
ISSN (online)	1095-9130
ISSN	1046-2023
DOI	10.1016/j.ymeth.2011.06.003
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Article ; Online: FACT and the H2B N Tail

Osley, Mary Ann

Molecular and Cellular Biology. 2014 Feb. 1, v. 34, no. 3 p.300-302

2014

Abstract	The FACT histone chaperone/nucleosome reorganization factor plays key roles in nucleosome dynamics during transcription. A new study has linked a specific domain in the H2B N terminus to the activity of FACT in regulating nucleosome disassembly at promoters during transcription activation and nucleosome reassembly at coding regions during transcription elongation.
Keywords	histones ; nucleosomes ; transcriptional activation
Language	English
Dates of publication	2014-0201
Size	p. 300-302.
Publishing place	Taylor & Francis
Document type	Article ; Online
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.01519-13
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Zs.A 1666: Show issues

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Article ; Online: Regulation of UV damage repair in quiescent yeast cells.

Long, Lindsey J / Lee, Po-Hsuen / Small, Eric M / Hillyer, Cory / Guo, Yan / Osley, Mary Ann

DNA repair

2020 Volume 90, Page(s) 102861

Abstract: Non-growing quiescent cells face special challenges when repairing lesions produced by exogenous DNA damaging agents. These challenges include the global repression of transcription and translation and a compacted chromatin structure. We investigated how ...

Abstract	Non-growing quiescent cells face special challenges when repairing lesions produced by exogenous DNA damaging agents. These challenges include the global repression of transcription and translation and a compacted chromatin structure. We investigated how quiescent yeast cells regulated the repair of DNA lesions produced by UV irradiation. We found that UV lesions were excised and repaired in quiescent cells before their re-entry into S phase, and that lesion repair was correlated with high levels of Rad7, a recognition factor in the global genome repair sub-pathway of nucleotide excision repair (GGR-NER). UV exposure led to an increased frequency of mutations that included C->T transitions and T > A transversions. Mutagenesis was dependent on the error-prone translesion synthesis (TLS) DNA polymerase, Pol zeta, which was the only DNA polymerase present in detectable levels in quiescent cells. Across the genome of quiescent cells, UV-induced mutations showed an association with exons that contained H3K36 or H3K79 trimethylation but not with those bound by RNA polymerase II. Together, the data suggest that the distinct physiological state and chromatin structure of quiescent cells contribute to its regulation of UV damage repair.
MeSH term(s)	Cell Cycle ; DNA Damage ; DNA Repair ; DNA, Fungal/metabolism ; DNA, Fungal/radiation effects ; DNA-Binding Proteins/metabolism ; DNA-Directed DNA Polymerase/metabolism ; Mutagenesis ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae/radiation effects ; Saccharomyces cerevisiae Proteins/metabolism ; Ultraviolet Rays
Chemical Substances	DNA, Fungal ; DNA-Binding Proteins ; RAD7 protein, S cerevisiae ; Saccharomyces cerevisiae Proteins ; DNA-Directed DNA Polymerase (EC 2.7.7.7)
Language	English
Publishing date	2020-04-30
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2071608-4
ISSN	1568-7856 ; 1568-7864
ISSN (online)	1568-7856
ISSN	1568-7864
DOI	10.1016/j.dnarep.2020.102861
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Article ; Online: Epigenetics: how to lose a tail.

Osley, Mary Ann

Nature

2008 Volume 456, Issue 7224, Page(s) 885–886

MeSH term(s)	Animals ; Cell Differentiation ; Chromatin/genetics ; Chromatin/metabolism ; Chromatin Assembly and Disassembly ; Embryonic Stem Cells/metabolism ; Epistasis, Genetic ; Histones/chemistry ; Histones/genetics ; Histones/metabolism ; Tetrahymena/genetics ; Tetrahymena/metabolism ; Yeasts/genetics ; Yeasts/metabolism
Chemical Substances	Chromatin ; Histones
Language	English
Publishing date	2008-12-18
Publishing country	England
Document type	News
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/456885a
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