MISC

2011年7月

Methylation analysis of circadian clock gene promoters in forensic autopsy specimens

LEGAL MEDICINE
  • Masato Nakatome
  • ,
  • Minami Orii
  • ,
  • Makoto Hamajima
  • ,
  • Yukari Hirata
  • ,
  • Misato Uemura
  • ,
  • Sayaka Hirayama
  • ,
  • Ichiro Isobe

13
4
開始ページ
205
終了ページ
209
記述言語
英語
掲載種別
DOI
10.1016/j.legalmed.2011.03.001
出版者・発行元
ELSEVIER IRELAND LTD

DNA methylation in gene promoter regions influences gene expression. Circadian clock genes play an important role in the formation of a biological clock and aberrant methylation of these genes contributes to several disorders. In this study, we examined forensic autopsy specimens to determine whether DNA methylation status in the promoter regions of nine circadian clock genes (Per1, Per2, Per3, Cry1, Cry2, Bmal1, Clock, Tim, and Ck1e) is related to a change in acquired diathesis and/or causes of death. Methylation-specific PCR and direct sequencing methods revealed that the promoters of Per1, Cry2, Bmal1, Clock, and Ck1e were unmethylated in all the forensic autopsy specimens, while the promoters of Per2, Per3, Cry1, and Tim were partially methylated. Methylation status varied between individuals and between tissues in the same patient. A detailed analysis of methylation patterns in the Cry1 promoter region revealed that the patterns also varied between individuals and the Cry1 promoter had highly methylated patterns in two cases that had been exposed to methamphetamine. These results suggest that the methylation status of clock gene promoters varies between individuals. Methamphetamine use may influence methylation in the Cry1 gene promoter region and disturb circadian rhythmicity. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.legalmed.2011.03.001
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000291776000009&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.legalmed.2011.03.001
  • ISSN : 1344-6223
  • Web of Science ID : WOS:000291776000009

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