Open AccessThe regulatory effect of acetylation of HMGN2 and H3K27 on pyocyanin‐induced autophagy in macrophages by affecting Ulk1 transcription
Author(s) -
Du Yu,
Guo Hongjun,
Guo Lijuan,
Miao Junming,
Ren Hongyu,
Liu Keyun,
Ren Laibin,
He Jinchen,
Wang Xiaoying,
Chen Junli,
Li Jingyu,
Wang Yi,
Wang Ji,
Huang Ning
Publication year - 2021
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.16788
Subject(s) - autophagy , acetylation , microbiology and biotechnology , pyocyanin , transcription factor , ulk1 , histone , pcaf , chemistry , transcription (linguistics) , death associated protein 6 , virulence , biology , biochemistry , nuclear protein , kinase , gene , apoptosis , protein kinase a , quorum sensing , linguistics , philosophy , ampk
Pyocyanin (PYO) is a major virulence factor secreted by Pseudomonas aeruginosa , and autophagy is a crucial homeostatic mechanism for the interaction between the pathogens and the host. It remains unknown whether PYO leads to autophagy in macrophages by regulating histone acetylation. The high mobility group nucleosomal binding domain 2 (HMGN2) has been reported to regulate the PYO‐induced autophagy and oxidative stress in the epithelial cells; however, the underlying molecular mechanism has not been fully elucidated. In this study, PYO was found to induce autophagy in macrophages, and the mechanism might be correlated with the up‐regulation of HMGN2 acetylation (HMGN2ac) and the down‐regulation of H3K27 acetylation (H3K27ac) by modulation of the activities of acetyltransferases and deacetylases. Moreover, we further demonstrated that the up‐regulated HMGN2ac enhances its recruitment to the Ulk1 promoter, while the down‐regulation of H3K27ac reduces its recruitment to the Ulk1 promoter, thereby promoting or inhibiting the transcription of Ulk1 . In conclusion, HMGN2ac and H3K27ac play regulatory roles in the PYO‐induced autophagy in macrophages.