Dual modes of DNA N <sup>6</sup> -methyladenine maintenance by distinct methyltransferase complexes

Y Yuanyuan Wang B Bei Nan (Key Laboratory of Evolution & Marine Biodiversity (Ministry of Education) and Institute of Evolution & Marine Biodiversity, Ocean University of China) F Fei Ye Z Zhe Zhang W Wentao Yang (Department of Biochemistry & Molecular Medicine, University of Southern California Keck School of Medicine) B Bo Pan F Fan Wei L Lili Duan (Key Laboratory of Evolution & Marine Biodiversity (Ministry of Education) and Institute of Evolution & Marine Biodiversity, Ocean University of China) H Haicheng Li (Center for Flexible Electronics Technology, Tsinghua University, No. 30, Shuangqing Road, Beijing 100084, People’s Republic of China) J Junhua Niu (Key Laboratory of Evolution & Marine Biodiversity (Ministry of Education) and Institute of Evolution & Marine Biodiversity, Ocean University of China) A Aili Ju (Key Laboratory of Evolution & Marine Biodiversity (Ministry of Education) and Institute of Evolution & Marine Biodiversity, Ocean University of China) Y Yongqiang Liu (Key Laboratory of Evolution & Marine Biodiversity (Ministry of Education) and Institute of Evolution & Marine Biodiversity, Ocean University of China) D Dantong Wang (BGI Research) W Wenxin Zhang (Institute of Biomedical Research, Yunnan University) Y Yifan Liu (State Key Laboratory of Coordination Chemistry, School of Chemistry and Chemical Engineering) S Shan Gao

Abstract

Stable inheritance of DNA N 6 -methyladenine (6mA) is crucial for its biological functions in eukaryotes. Here, we identify two distinct methyltransferase (MTase) complexes, both sharing the catalytic subunit AMT1, but featuring AMT6 and AMT7 as their unique components, respectively. While the two complexes are jointly responsible for 6mA maintenance methylation, they exhibit distinct enzymology, DNA/chromatin affinity, genomic distribution, and knockout phenotypes. AMT7 complex, featuring high MTase activity and processivity, is connected to transcription-associated epigenetic marks, including H2A.Z and H3K4me3, and is required for the bulk of maintenance methylation. In contrast, AMT6 complex, with reduced activity and processivity, is recruited by PCNA to initiate maintenance methylation immediately after DNA replication. These two complexes coordinate in maintenance methylation. By integrating signals from both replication and transcription, this mechanism ensures the faithful and efficient transmission of 6mA as an epigenetic mark in eukaryotes.

Article Details

Volume / Issue Vol. 122, Issue 3
Published January 21, 2025
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (16)

Y

Yuanyuan Wang

B

Bei Nan

Key Laboratory of Evolution & Marine Biodiversity (Ministry of Education) and Institute of Evolution & Marine Biodiversity, Ocean University of China

F

Fei Ye

Z

Zhe Zhang

W

Wentao Yang

Department of Biochemistry & Molecular Medicine, University of Southern California Keck School of Medicine

B

Bo Pan

F

Fan Wei

L

Lili Duan

Key Laboratory of Evolution & Marine Biodiversity (Ministry of Education) and Institute of Evolution & Marine Biodiversity, Ocean University of China

H

Haicheng Li

Center for Flexible Electronics Technology, Tsinghua University, No. 30, Shuangqing Road, Beijing 100084, People’s Republic of China

J

Junhua Niu

Key Laboratory of Evolution & Marine Biodiversity (Ministry of Education) and Institute of Evolution & Marine Biodiversity, Ocean University of China

A

Aili Ju

Key Laboratory of Evolution & Marine Biodiversity (Ministry of Education) and Institute of Evolution & Marine Biodiversity, Ocean University of China

Y

Yongqiang Liu

Key Laboratory of Evolution & Marine Biodiversity (Ministry of Education) and Institute of Evolution & Marine Biodiversity, Ocean University of China

D

Dantong Wang

BGI Research

W

Wenxin Zhang

Institute of Biomedical Research, Yunnan University

Y

Yifan Liu

State Key Laboratory of Coordination Chemistry, School of Chemistry and Chemical Engineering

S

Shan Gao