Genome-wide analysis of abnormal H3K9 acetylation in cloned mice.

Somatic nuclear transfer is a cloning technique that shows great promise in the application to regenerative medicine. Although cloned animals are genetically identical to their donor counterparts, abnormalities in phenotype and gene expression are frequently observed. One hypothesis is that the caus...

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Autores principales:	Takahiro Suzuki, Shinji Kondo, Teruhiko Wakayama, Paul E Cizdziel, Yoshihide Hayashizaki
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2008
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c3bee36399f14448b16eb1d8261c3741
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spelling	oai:doaj.org-article:c3bee36399f14448b16eb1d8261c37412021-11-25T06:12:53ZGenome-wide analysis of abnormal H3K9 acetylation in cloned mice.1932-620310.1371/journal.pone.0001905https://doaj.org/article/c3bee36399f14448b16eb1d8261c37412008-04-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18398451/?tool=EBIhttps://doaj.org/toc/1932-6203Somatic nuclear transfer is a cloning technique that shows great promise in the application to regenerative medicine. Although cloned animals are genetically identical to their donor counterparts, abnormalities in phenotype and gene expression are frequently observed. One hypothesis is that the cause of these abnormalities is due to epigenetic aberration. In this report, we focused our analysis on the acetylation of histone H3 at lysine9 (H3K9Ac). Through the use of whole genome tiling arrays and quantitative PCR, we examined this epigenetic event and directly compared and assessed the differences between a cloned mouse (C1) and its parental nuclear donor (D1) counterpart. We identified 4720 regions of chromosomal DNA that showed notable differences in H3K9Ac and report here many genes identified in these hyper- and hypo-acetylated regions. Analysis of a second clone (C2) and its parental donor counterpart (D2) for H3K9Ac showed a high degree of similarity to the C1/D1 pair. This conservation of aberrant acetylation is suggestive of a reproducible epigenetic phenomenon that may lead to the frequent abnormalities observed in cloned mice, such as obesity. Furthermore, we demonstrated Crp which was identified as a hyper-acetylated gene in this study is related to the body mass, suggesting that Crp is a possible candidate of a cause for the abnormal obesity in cloned mice. In this, one of the first reports describing genome-wide epigenetic aberration between parental and nuclear transfer-cloned mammals, we propose that aberrant acetylation of histones (H3K9Ac) flanking promoter regions highly correlates with gene-expression and may itself be an epigenetic change that accounts for variable expression patterns observed in cloned animals.Takahiro SuzukiShinji KondoTeruhiko WakayamaPaul E CizdzielYoshihide HayashizakiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 3, Iss 4, p e1905 (2008)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Takahiro Suzuki Shinji Kondo Teruhiko Wakayama Paul E Cizdziel Yoshihide Hayashizaki Genome-wide analysis of abnormal H3K9 acetylation in cloned mice.
description	Somatic nuclear transfer is a cloning technique that shows great promise in the application to regenerative medicine. Although cloned animals are genetically identical to their donor counterparts, abnormalities in phenotype and gene expression are frequently observed. One hypothesis is that the cause of these abnormalities is due to epigenetic aberration. In this report, we focused our analysis on the acetylation of histone H3 at lysine9 (H3K9Ac). Through the use of whole genome tiling arrays and quantitative PCR, we examined this epigenetic event and directly compared and assessed the differences between a cloned mouse (C1) and its parental nuclear donor (D1) counterpart. We identified 4720 regions of chromosomal DNA that showed notable differences in H3K9Ac and report here many genes identified in these hyper- and hypo-acetylated regions. Analysis of a second clone (C2) and its parental donor counterpart (D2) for H3K9Ac showed a high degree of similarity to the C1/D1 pair. This conservation of aberrant acetylation is suggestive of a reproducible epigenetic phenomenon that may lead to the frequent abnormalities observed in cloned mice, such as obesity. Furthermore, we demonstrated Crp which was identified as a hyper-acetylated gene in this study is related to the body mass, suggesting that Crp is a possible candidate of a cause for the abnormal obesity in cloned mice. In this, one of the first reports describing genome-wide epigenetic aberration between parental and nuclear transfer-cloned mammals, we propose that aberrant acetylation of histones (H3K9Ac) flanking promoter regions highly correlates with gene-expression and may itself be an epigenetic change that accounts for variable expression patterns observed in cloned animals.
format	article
author	Takahiro Suzuki Shinji Kondo Teruhiko Wakayama Paul E Cizdziel Yoshihide Hayashizaki
author_facet	Takahiro Suzuki Shinji Kondo Teruhiko Wakayama Paul E Cizdziel Yoshihide Hayashizaki
author_sort	Takahiro Suzuki
title	Genome-wide analysis of abnormal H3K9 acetylation in cloned mice.
title_short	Genome-wide analysis of abnormal H3K9 acetylation in cloned mice.
title_full	Genome-wide analysis of abnormal H3K9 acetylation in cloned mice.
title_fullStr	Genome-wide analysis of abnormal H3K9 acetylation in cloned mice.
title_full_unstemmed	Genome-wide analysis of abnormal H3K9 acetylation in cloned mice.
title_sort	genome-wide analysis of abnormal h3k9 acetylation in cloned mice.
publisher	Public Library of Science (PLoS)
publishDate	2008
url	https://doaj.org/article/c3bee36399f14448b16eb1d8261c3741
work_keys_str_mv	AT takahirosuzuki genomewideanalysisofabnormalh3k9acetylationinclonedmice AT shinjikondo genomewideanalysisofabnormalh3k9acetylationinclonedmice AT teruhikowakayama genomewideanalysisofabnormalh3k9acetylationinclonedmice AT paulecizdziel genomewideanalysisofabnormalh3k9acetylationinclonedmice AT yoshihidehayashizaki genomewideanalysisofabnormalh3k9acetylationinclonedmice
_version_	1718414068396589056

Genome-wide analysis of abnormal H3K9 acetylation in cloned mice.

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