[S8] 細菌エピジェネティクスとメタエピゲノミクス、DNAメチル化を中心に

[S8-5] DNAメチル化酵素の配列特異性変換に伴うピロリ菌エピゲノム・ミクロ進化

○福世 真樹¹，米澤 英雄²，今野 武津子³，柴田 朋子⁴，重信 秀治⁴，ラヒムトラ バハテヤリ¹，内山 郁夫⁴，金田 篤志¹，小林 一三⁵ (¹千葉大，²杏林大，³札幌厚生病院，⁴基生研，⁵法政大)

H. pylori lives in half of our stomach and may cause gastric cancer. Each strain has a large unique repertoire of DNA methyltransferases, that form a complex network for gene expression. Sequence-specificity changes in its methyltransferase may replace its branching edges to genes in a short evolutionary time scale. To examine such methylome micro-evolution, we compared strains from family members in genome and methylome (PacBio) and transcriptome (Illumina RNA-seq). In one family, a Type III methylation motif was found only in one strain. Here, expression of genes for virulence/host interaction (cagA, ureABC, amiE, hopCZ, sabA, cag16, lptG), co-factor metabolism (VB7/VB9, pdxA, hemH, modB, selA) and DNA reactions (uvrC, DNMT1) have changed. Another family have changes in many methylation motifs, some corresponding to a related set of Type I restriction-modification systems. We reconstructed evolution of the latter’s specificity subunit genes by a single bp substitution, intra-molecular deletion and gene conversion. Expression changes involved genes for virulence/host interaction (cagA, cag9, cag16, vacA, amiE, hopZ, fliCE), co-factor metabolism (VB9), DNA reactions (DNMT1, mutS-2, uvrD, ung, recG, ruvC, dnaAG, rnhB). Other co-authors: Hirokazu Yano⁶, Yukako Katsura⁷, Koji Yahara⁸, Yoshinori Hasegawa⁹, Osamu Ohara⁹. ⁶Tohoku U.; ⁷Kyoto U.; ⁸NIID; ⁹KDRI.