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生活里的创意|【科技前沿】专家点评：Andrew Z. Xiao/李海涛合作发现DNA 6mA润饰影响染色质结构…( 三 )


We do need to acknowledge that studies on 6mA have been set back by lack of knowledge about its potential source of contamination and sometimes just sloppy, irresponsible reports. Recent careful analysis of 6mA in mammalian gDNA is very important to bring cautions to the community and set the right course. With these cautions in mind, results have also been emerging to show notable presence of 6mA in mitochondrial DNA in mammals (https://www.cell.com/molecular-cell/pdfExtended/S1097-2765(20)30111-8), unpublished results indicating increased and detectable gDNA 6mA in mammalian cells under stress from us and other, and now the very nice study by Xiao and Li laboratories and their collaborators reporting the presence of 6mA at regions of SIDD. The authors showed strong evidence supporting the presence of 6mA at these regions in mouse trophoblast stem cells. They have further shown that SATB1, a protein interacts with SIDD, exhibits 500-fold difference in DNA binding with or without 6mA. The authors thus propose functional roles of 6mA-mediated regulation in chromatin domain separation during early embryo development. Different from 5mC, the presence of 6mA destabilizes Watson-Crick base pairing. The presence of 6mA at DNA repeat elements is very likely a mechanism to destabilize dsDNA. Transition from dsDNA to ssDNA or equilibrium between dsDNA and ssDNA have been proposed as another layer of genome regulation. 6mA could uniquely fit this role.
【生活里的创意|【科技前沿】专家点评：Andrew Z. Xiao/李海涛合作发现DNA 6mA润饰影响染色质结构…】Many challenges remain exist to provide fully convincing evidence that 6mA is doing what has been proposed. On top of the lists are two main challenges: i) identification of the methyltransferase that mediates gDNA 6mA methylation; ii) a truly quantitative sequencing method that can convincingly read out the exact local and modification level at each 6mA modified site. METTL4 can mediate mitochondrial DNA methylation. Presence of other methyltransferases for mtDNA and gDNA is possible. A truly quantitative method will really open up the entire field.
原文链接：
https://doi.org/10.1038/s41586-020-2500-9
制版人：MENG
参考文献
1. Fu, Y., Luo, G.Z., Chen, K., Deng, X., Yu, M., Han, D., Hao, Z., Liu, J., Lu, X.,Dore, L.C., et al. (2015). N6-methyldeoxyadenosine marks active transcription start sites in Chlamydomonas. Cell 161, 879–892.
2. Zhang, G., Huang, H., Liu, D., Cheng, Y., Liu, X., Zhang, W., Yin, R., Zhang, D.,Zhang, P., Liu, J., et al. (2015). N6-methyladenine DNA modification in Drosophila. Cell 161, 893–906.
3. Greer, E.L., Blanco, M.A., Gu, L., Sendinc, E., Liu, J., Aristiza bal-Corrales, D., Hsu, C.H., Aravind, L., He, C., and Shi, Y. (2015). DNA methylation on N6- adenine in C. elegans. Cell 161, 868–878.
4. T. P. Wu, T. Wang, M. G. Seetin, Y. Lai, S. Zhu, K. Lin, Y. Liu, S. D. Byrum, S. G. Mackintosh, M. Zhong, A. Tackett, G. Wang, L. S. Hon, G. Fang, J. A. Swenberg, A. Z. Xiao, DNA methylation on N6-adenine in mammalian embryonic stem cells. Nature 532, 329–333 (2016)


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