Post-translational regulation of autophagy is involved in intra-microbiome suppression of fungal pathogens

Microbiome

Qiming Sun¹  Yunrong Chai²  Jinrong Xu³  Gabriele Berg⁴  Tomislav Cernava⁴  Jing Wang⁵  Yun Chen⁵  Chaoyun Xu⁵  Zhonghua Ma⁵ 

[1] Department of Biochemistry, and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, 310058, Hangzhou, China;Department of Biology, Northeastern University, Boston, MA, USA;Department of Botany and Plant Pathology, Purdue University, West Lafayette, IN, USA;Institute of Environmental Biotechnology, Graz University of Technology, Graz, Austria;State Key Laboratory of Rice Biology, and Key Laboratory of Molecular Biology of Crop Pathogens and Insects, Institute of Biotechnology, Zhejiang University, 866 Yuhangtang Road, 310058, Hangzhou, China;

关键词: Intra-microbiome;    Bacterial–fungal interaction;    Autophagy;    Post-translational regulation;    Acetylation;    Fusarium graminearum;    Streptomyces hygroscopicus;   

DOI  :  10.1186/s40168-021-01077-y

来源: Springer

【 摘 要 】

BackgroundMicrobiome interactions are important determinants for ecosystem functioning, stability, and health. In previous studies, it was often observed that bacteria suppress potentially pathogenic fungal species that are part of the same plant microbiota; however, the underlying microbe-microbe interplay remains mostly elusive. Here, we explored antagonistic interactions of the fungus Fusarium graminearum and bacterium Streptomyces hygroscopicus at the molecular level. Both are ubiquitous members of the healthy wheat microbiota; under dysbiosis, the fungus causes devastating diseases.ResultsIn co-cultures, we found that Streptomyces alters the fungal acetylome leading to substantial induction of fungal autophagy. The bacterium secrets rapamycin to inactivate the target of rapamycin (TOR), which subsequently promotes the degradation of the fungal histone acetyltransferase Gcn5 through the 26S proteasome. Gcn5 negatively regulates fungal autophagy by acetylating the autophagy-related protein Atg8 at the lysine site K13 and blocking cellular relocalization of Atg8. Thus, degradation of Gcn5 triggered by rapamycin was found to reduce Atg8 acetylation, resulting in autophagy induction in F. graminearum.ConclusionsAutophagy homeostasis plays an essential role in fungal growth and competition, as well as for virulence. Our work reveals a novel post-translational regulation of autophagy initiated by a bacterial antibiotic. Rapamycin was shown to be a powerful modulator of bacteria–fungi interactions with potential importance in explaining microbial homeostasis in healthy plant microbiomes. The autophagic process provides novel possibilities and targets to biologically control pathogens.3Zu6EQMv78RbwrwJHF2G1TVideo abstract

【 授权许可】

CC BY