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Article: Pathologic Replication-Independent Endogenous DNA Double-Strand Breaks Repair Defect in Chronological Aging Yeast.

Pongpanich, Monnat / Patchsung, Maturada / Mutirangura, Apiwat

2018 Volume 9, Page(s) 501

Abstract: Reduction of physiologic replication-independent endogenous DNA double strand breaks (Phy-RIND-EDSBs) in chronological aging yeast increases pathologic RIND-EDSBs (Path-RIND-EDSBs). Path-RIND-EDSBs can occur spontaneously in non-dividing cells without ... ...

Abstract	Reduction of physiologic replication-independent endogenous DNA double strand breaks (Phy-RIND-EDSBs) in chronological aging yeast increases pathologic RIND-EDSBs (Path-RIND-EDSBs). Path-RIND-EDSBs can occur spontaneously in non-dividing cells without any inductive agents, and they must be repaired immediately otherwise their accumulation can lead to senescence. If yeasts have DSB repair defect, retention of Path-RIND-EDSBs can be found. Previously, we found that Path-RIND-EDSBs are not only produced but also retained in chronological aging yeast. Here, we evaluated if chronological aging yeasts have a DSB repair defect. We found a significant accumulation of Path-RIND-EDSBs around the same level in aging cells and caffeine treated cells and at a much higher level in the DSB repair mutant cells. Especially in the mutant, some unknown sequence was found inserted at the breaks. In addition, % difference of cell viability between HO induced and non-induced cells was significantly greater in aging cells. Our results suggested that RIND-EDSBs repair efficiency declines, but is not absent, in chronological aging yeast which might promote senescence phenotype. When a repair protein is deficient, an alternative pathway might be employed or an end modification process might occur as inserted sequences at the breaks were observed. Restoring repair defects might slow down the deterioration of cells from chronological aging.
Language	English
Publishing date	2018-10-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2018.00501
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Article ; Online: The association between Alu hypomethylation and severity of type 2 diabetes mellitus.

Thongsroy, Jirapan / Patchsung, Maturada / Mutirangura, Apiwat

Clinical epigenetics

2017 Volume 9, Page(s) 93

Abstract: Background: Cellular senescence due to genomic instability is believed to be one of the mechanisms causing health problems in diabetes mellitus (DM). Low methylation levels of Alu elements or Alu hypomethylation, an epigenomic event causing genomic ... ...

Abstract	Background: Cellular senescence due to genomic instability is believed to be one of the mechanisms causing health problems in diabetes mellitus (DM). Low methylation levels of Alu elements or Alu hypomethylation, an epigenomic event causing genomic instability, were commonly found in aging people and patients with aging phenotypes, such as osteoporosis. Results: We investigate Alu methylation levels of white blood cells of type 2 DM, pre-DM, and control. The DM group possess the lowest Alu methylation ( Conclusion: Genome-wide hypomethylation may be one of the underlining mechanisms causing genomic instability in type 2 DM. Moreover, Alu methylation levels may be a useful biomarker for monitoring cellular senescence in type 2 DM patients.
Language	English
Publishing date	2017
Publishing country	Germany
Document type	Journal Article
ISSN	1868-7083
ISSN (online)	1868-7083
DOI	10.1186/s13148-017-0395-6
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Article ; Online: Reduction in replication-independent endogenous DNA double-strand breaks promotes genomic instability during chronological aging in yeast.

Thongsroy, Jirapan / Patchsung, Maturada / Pongpanich, Monnat / Settayanon, Sirapat / Mutirangura, Apiwat

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2018 , Page(s) fj201800218RR

Abstract: The mechanism that causes genomic instability in nondividing aging cells is unknown. Our previous study of mutant yeast suggested that 2 types of replication-independent endogenous DNA double-strand breaks (RIND-EDSBs) exist and that they play opposing ... ...

Abstract	The mechanism that causes genomic instability in nondividing aging cells is unknown. Our previous study of mutant yeast suggested that 2 types of replication-independent endogenous DNA double-strand breaks (RIND-EDSBs) exist and that they play opposing roles. The first type, known as physiologic RIND-EDSBs, were ubiquitous in the G
Language	English
Publishing date	2018-05-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.201800218RR
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Article ; Online: The association between Alu hypomethylation and severity of type 2 diabetes mellitus

Jirapan Thongsroy / Maturada Patchsung / Apiwat Mutirangura

Clinical Epigenetics, Vol 9, Iss 1, Pp 1-

2017 Volume 9

Abstract: Abstract Background Cellular senescence due to genomic instability is believed to be one of the mechanisms causing health problems in diabetes mellitus (DM). Low methylation levels of Alu elements or Alu hypomethylation, an epigenomic event causing ... ...

Abstract	Abstract Background Cellular senescence due to genomic instability is believed to be one of the mechanisms causing health problems in diabetes mellitus (DM). Low methylation levels of Alu elements or Alu hypomethylation, an epigenomic event causing genomic instability, were commonly found in aging people and patients with aging phenotypes, such as osteoporosis. Results We investigate Alu methylation levels of white blood cells of type 2 DM, pre-DM, and control. The DM group possess the lowest Alu methylation (P < 0.001, P < 0.0001 adjusted age). In the DM group, Alu hypomethylation is directly correlated with high fasting blood sugar, HbA1C, and blood pressure. Conclusion Genome-wide hypomethylation may be one of the underlining mechanisms causing genomic instability in type 2 DM. Moreover, Alu methylation levels may be a useful biomarker for monitoring cellular senescence in type 2 DM patients.
Keywords	DNA methylation ; Diabetes mellitus ; Genomic instability ; Alu ; Senescence ; Medicine ; R ; Genetics ; QH426-470
Language	English
Publishing date	2017-08-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article ; Online: Alu siRNA to increase Alu element methylation and prevent DNA damage.

Patchsung, Maturada / Settayanon, Sirapat / Pongpanich, Monnat / Mutirangura, Dharm / Jintarith, Pornrutsami / Mutirangura, Apiwat

Epigenomics

2018 Volume 10, Issue 2, Page(s) 175–185

Abstract: Global DNA hypomethylation promoting genomic instability leads to cancer and deterioration of human health with age.: Aim: To invent a biotechnology that can reprogram this process.: Methods: We used Alu siRNA to direct Alu interspersed repetitive ... ...

Abstract	Global DNA hypomethylation promoting genomic instability leads to cancer and deterioration of human health with age. Aim: To invent a biotechnology that can reprogram this process. Methods: We used Alu siRNA to direct Alu interspersed repetitive sequences methylation in human cells. We evaluated the correlation between DNA damage and Alu methylation levels. Results: We observed an inverse correlation between Alu element methylation and endogenous DNA damage in white blood cells. Cells transfected with Alu siRNA exhibited high Alu methylation levels, increased proliferation, reduced endogenous DNA damage and improved resistance to DNA damaging agents. Conclusion: Alu methylation stabilizes the genome by preventing accumulation of DNA damage. Alu siRNA could be useful for evaluating reprograming of the global hypomethylation phenotype in cancer and aging cells.
MeSH term(s)	Aging ; Alu Elements ; DNA Damage ; DNA Methylation ; Genomic Instability ; Humans ; Interspersed Repetitive Sequences ; RNA, Small Interfering
Chemical Substances	RNA, Small Interfering
Language	English
Publishing date	2018-01-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1750-192X
ISSN (online)	1750-192X
DOI	10.2217/epi-2017-0096
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Article ; Online: Discovery and Genetic Code Expansion of a Polyethylene Terephthalate (PET) Hydrolase from the Human Saliva Metagenome for the Degradation and Bio-Functionalization of PET.

Eiamthong, Bhumrapee / Meesawat, Piyachat / Wongsatit, Thanakrit / Jitdee, Jariya / Sangsri, Raweewan / Patchsung, Maturada / Aphicho, Kanokpol / Suraritdechachai, Surased / Huguenin-Dezot, Nicolas / Tang, Shan / Suginta, Wipa / Paosawatyanyong, Boonchoat / Babu, M Madan / Chin, Jason W / Pakotiprapha, Danaya / Bhanthumnavin, Worawan / Uttamapinant, Chayasith

Angewandte Chemie (International ed. in English)

2022 Volume 61, Issue 37, Page(s) e202203061

Abstract: We report a bioinformatic workflow and subsequent discovery of a new polyethylene terephthalate (PET) hydrolase, which we named MG8, from the human saliva metagenome. MG8 has robust PET plastic degradation activities under different temperature and ... ...

Abstract	We report a bioinformatic workflow and subsequent discovery of a new polyethylene terephthalate (PET) hydrolase, which we named MG8, from the human saliva metagenome. MG8 has robust PET plastic degradation activities under different temperature and salinity conditions, outperforming several naturally occurring and engineered hydrolases in degrading PET. Moreover, we genetically encoded 2,3-diaminopropionic acid (DAP) in place of the catalytic serine residue of MG8, thereby converting a PET hydrolase into a covalent binder for bio-functionalization of PET. We show that MG8(DAP), in conjunction with a split green fluorescent protein system, can be used to attach protein cargos to PET as well as other polyester plastics. The discovery of a highly active PET hydrolase from the human metagenome-currently an underexplored resource for industrial enzyme discovery-as well as the repurposing of such an enzyme into a plastic functionalization tool, should facilitate ongoing efforts to degrade and maximize reusability of PET.
MeSH term(s)	Genetic Code ; Humans ; Hydrolases/metabolism ; Metagenome ; Plastics/chemistry ; Polyethylene Terephthalates/chemistry ; Saliva/metabolism
Chemical Substances	Plastics ; Polyethylene Terephthalates ; Hydrolases (EC 3.-)
Language	English
Publishing date	2022-06-21
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2011836-3
ISSN	1521-3773 ; 1433-7851
ISSN (online)	1521-3773
ISSN	1433-7851
DOI	10.1002/anie.202203061
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Article ; Online: Characteristics of replication-independent endogenous double-strand breaks in Saccharomyces cerevisiae.

Pongpanich, Monnat / Patchsung, Maturada / Thongsroy, Jirapan / Mutirangura, Apiwat

BMC genomics

2014 Volume 15, Page(s) 750

Abstract: Background: Replication-independent endogenous double-strand breaks (RIND-EDSBs) occur in both humans and yeast in the absence of inductive agents and DNA replication. In human cells, RIND-EDSBs are hypermethylated, preferentially retained in the ... ...

Abstract	Background: Replication-independent endogenous double-strand breaks (RIND-EDSBs) occur in both humans and yeast in the absence of inductive agents and DNA replication. In human cells, RIND-EDSBs are hypermethylated, preferentially retained in the heterochromatin and unbound by γ-H2AX. In single gene deletion yeast strains, the RIND-EDSB levels are altered; the number of RIND-EDSBs is higher in strains with deletions of histone deacetylase, endonucleases, topoisomerase, or DNA repair regulators, but lower in strains with deletions of the high-mobility group box proteins or Sir2. In summary, RIND-EDSBs are different from pathologic DSBs in terms of their causes and consequences. In this study, we identified the nucleotide sequences surrounding RIND-EDSBs and investigated the features of these sequences as well as their break locations. Results: In recent work, we detected RIND-EDSBs using ligation mediated PCR. In this study, we sequenced RIND-EDSB PCR products of resting state Saccharomyces cerevisiae using next-generation sequencing to analyze RIND-EDSB sequences. We found that the break locations are scattered across a number of chromosomes. The number of breaks correlated with the size of the chromosomes. Most importantly, the break occurrences had sequence pattern specificity. Specifically, the majority of the breaks occurred immediately after the sequence "ACGT" (P = 2.2E-156). Because the "ACGT" sequence does not occur primarily in the yeast genome, this specificity of the "ACGT" sequence cannot be attributed to chance. Conclusions: RIND-EDSBs occur non-randomly; that is, they are produced and retained by specific mechanisms. Because these particular mechanisms regulate their generation and they possess potentially specific functions, RIND-EDSBs could be epigenetic marks.
MeSH term(s)	Base Sequence ; Chromosome Mapping ; Chromosomes, Fungal/genetics ; DNA Breaks, Double-Stranded ; DNA Repair ; DNA Replication ; DNA, Fungal/genetics ; Genes, Fungal ; Molecular Sequence Data ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae Proteins/genetics
Chemical Substances	DNA, Fungal ; Saccharomyces cerevisiae Proteins
Language	English
Publishing date	2014-09-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1471-2164
ISSN (online)	1471-2164
DOI	10.1186/1471-2164-15-750
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Article: Argonaute 4 as an Effector Protein in RNA-Directed DNA Methylation in Human Cells.

Chalertpet, Kanwalat / Pin-On, Piyapat / Aporntewan, Chatchawit / Patchsung, Maturada / Ingrungruanglert, Praewphan / Israsena, Nipan / Mutirangura, Apiwat

Frontiers in genetics

2019 Volume 10, Page(s) 645

Abstract: DNA methylation of specific genome locations contributes to the distinct functions of multicellular organisms. DNA methylation can be governed by RNA-dependent DNA methylation (RdDM). RdDM is carried out by endogenous small-RNA-guided epigenomic editing ... ...

Abstract	DNA methylation of specific genome locations contributes to the distinct functions of multicellular organisms. DNA methylation can be governed by RNA-dependent DNA methylation (RdDM). RdDM is carried out by endogenous small-RNA-guided epigenomic editing complexes that add a methyl group to a precise DNA location. In plants, the Argonaute 4 (AGO4) protein is one of the main catalytic components involved in RdDM. Although small interfering RNA or short hairpin RNA has been shown to be able to guide DNA methylation in human cells, AGO protein-regulated RdDM in humans has not yet been evaluated. This study aimed to identify a key regulatory AGO protein involved in human RdDM by bioinformatics and to explore its function in RdDM by a combination of AGO4 knockdown, Alu small interfering RNA transfection, AGO4-expressing plasmid transfection, chromatin immunoprecipitation, cell-penetrating peptide-tagged AGO4 combined Alu single-guide RNA transfection, and methylation analyses. We found that first, human AGO4 showed stronger genome-wide association with DNA methylation than AGO1-AGO3. Second, endogenous AGO4 depletion demethylated DNA of known AGO4 bound loci. Finally, exogenous AGO4
Language	English
Publishing date	2019-07-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2019.00645
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Article ; Online: The roles of HMGB1-produced DNA gaps in DNA protection and aging biomarker reversal.

Yasom, Sakawdaurn / Watcharanurak, Papitchaya / Bhummaphan, Narumol / Thongsroy, Jirapan / Puttipanyalears, Charoenchai / Settayanon, Sirapat / Chalertpet, Kanwalat / Khumsri, Wilunplus / Kongkaew, Aphisek / Patchsung, Maturada / Siriwattanakankul, Chutha / Pongpanich, Monnat / Pin-On, Piyapat / Jindatip, Depicha / Wanotayan, Rujira / Odton, Mingkwan / Supasai, Suangsuda / Oo, Thura Tun / Arunsak, Busarin /

Pratchayasakul, Wasana / Chattipakorn, Nipon / Chattipakorn, Siriporn / Mutirangura, Apiwat

FASEB bioAdvances

2022 Volume 4, Issue 6, Page(s) 408–434

Abstract: The endogenous DNA damage triggering an aging progression in the elderly is prevented in the youth, probably by naturally occurring DNA gaps. Decreased DNA gaps are found during chronological aging in yeast. So we named the gaps "Youth-DNA-GAPs." The ... ...

Abstract	The endogenous DNA damage triggering an aging progression in the elderly is prevented in the youth, probably by naturally occurring DNA gaps. Decreased DNA gaps are found during chronological aging in yeast. So we named the gaps "Youth-DNA-GAPs." The gaps are hidden by histone deacetylation to prevent DNA break response and were also reduced in cells lacking either the high-mobility group box (HMGB) or the NAD-dependent histone deacetylase, SIR2. A reduction in DNA gaps results in shearing DNA strands and decreasing cell viability. Here, we show the roles of DNA gaps in genomic stability and aging prevention in mammals. The number of Youth-DNA-GAPs were low in senescent cells, two aging rat models, and the elderly. Box A domain of HMGB1 acts as molecular scissors in producing DNA gaps. Increased gaps consolidated DNA durability, leading to DNA protection and improved aging features in senescent cells and two aging rat models similar to those of young organisms. Like the naturally occurring Youth-DNA-GAPs, Box A-produced DNA gaps avoided DNA double-strand break response by histone deacetylation and SIRT1, a Sir2 homolog. In conclusion, Youth-DNA-GAPs are a biomarker determining the DNA aging stage (young/old). Box A-produced DNA gaps ultimately reverse aging features. Therefore, DNA gap formation is a potential strategy to monitor and treat aging-associated diseases.
Language	English
Publishing date	2022-03-28
Publishing country	United States
Document type	Journal Article
ISSN	2573-9832
ISSN (online)	2573-9832
DOI	10.1096/fba.2021-00131
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Article ; Online: The roles of HMGB1‐produced DNA gaps in DNA protection and aging biomarker reversal

Sakawdaurn Yasom / Papitchaya Watcharanurak / Narumol Bhummaphan / Jirapan Thongsroy / Charoenchai Puttipanyalears / Sirapat Settayanon / Kanwalat Chalertpet / Wilunplus Khumsri / Aphisek Kongkaew / Maturada Patchsung / Chutha Siriwattanakankul / Monnat Pongpanich / Piyapat Pin‐on / Depicha Jindatip / Rujira Wanotayan / Mingkwan Odton / Suangsuda Supasai / Thura Tun Oo / Busarin Arunsak /

Wasana Pratchayasakul / Nipon Chattipakorn / Siriporn Chattipakorn / Apiwat Mutirangura

FASEB BioAdvances, Vol 4, Iss 6, Pp 408-

2022 Volume 434

Abstract: Abstract The endogenous DNA damage triggering an aging progression in the elderly is prevented in the youth, probably by naturally occurring DNA gaps. Decreased DNA gaps are found during chronological aging in yeast. So we named the gaps “Youth‐DNA‐GAPs.” ...

Abstract	Abstract The endogenous DNA damage triggering an aging progression in the elderly is prevented in the youth, probably by naturally occurring DNA gaps. Decreased DNA gaps are found during chronological aging in yeast. So we named the gaps “Youth‐DNA‐GAPs.” The gaps are hidden by histone deacetylation to prevent DNA break response and were also reduced in cells lacking either the high‐mobility group box (HMGB) or the NAD‐dependent histone deacetylase, SIR2. A reduction in DNA gaps results in shearing DNA strands and decreasing cell viability. Here, we show the roles of DNA gaps in genomic stability and aging prevention in mammals. The number of Youth‐DNA‐GAPs were low in senescent cells, two aging rat models, and the elderly. Box A domain of HMGB1 acts as molecular scissors in producing DNA gaps. Increased gaps consolidated DNA durability, leading to DNA protection and improved aging features in senescent cells and two aging rat models similar to those of young organisms. Like the naturally occurring Youth‐DNA‐GAPs, Box A‐produced DNA gaps avoided DNA double‐strand break response by histone deacetylation and SIRT1, a Sir2 homolog. In conclusion, Youth‐DNA‐GAPs are a biomarker determining the DNA aging stage (young/old). Box A‐produced DNA gaps ultimately reverse aging features. Therefore, DNA gap formation is a potential strategy to monitor and treat aging‐associated diseases.
Keywords	aging ; DNA damage ; DNA gap ; rejuvenation ; RIND‐EDSB ; senescence ; Biology (General) ; QH301-705.5
Subject code	612
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
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