|
|||||
|
|
An epigenetic aberration increased in intergenic regions of cloned mice |
|
| Authors: | Hiromi Nishida Shinji Kondo Takahiro Suzuki Yuki Tsujimura Shunsuke Komatsu Teruhiko Wakayama Yoshihide Hayashizaki |
| Institution: | 1. Genome Exploration Research Group, RIKEN Genomic Sciences Center (GSC), Yokohama, Japan 2. Agricultural Bioinformatics Research Unit, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Tokyo, 113-8657, Japan 3. Division of Genomic Information Resources, Science of Biological Supramolecular Systems, Graduate School of Integrated Science, Yokohama City University, Yokohama, Japan 4. Laboratory for Genome Reprogramming, RIKEN Center for Developmental Biology (CDB), Kobe, Japan 5. Genome Science Laboratory, Discovery and Research Institute, RIKEN Wako Main Campus, Wako, Japan |
| Abstract: | The causes of frequent abnormal phenotypes and low success rate in mammalian cloning are poorly understood. Although epigenetic aberration is suspected to be a cause, its connection to the phenotypes has yet to be investigated. To measure the level of reprogramming of an epigenetic mark, acetylation at lysine 9 of histone H3 (H3K9Ac), in cloned mice, we examined its conservation between two cloned mice derived from distinct cell nuclei and their natural donors by utilizing whole-genome tiling arrays and quantitative PCR. Pairwise comparison of the H3K9Ac enrichment profile between the four mice revealed that H3K9Ac is less conserved in intergenic regions than in promoter regions of protein-coding genes. Intriguingly, the variation of H3K9Ac enrichment in intergenic regions is the most prominent in comparison of the two clones, possibly reflecting an additive effect of aberrant reprogramming of this epigenetic information occurring specifically in each of the two clones. |
| Keywords: | |
| 本文献已被 SpringerLink 等数据库收录！ | |