Nature communications · 2024
Legionella maintains host cell ubiquitin homeostasis by effectors with unique catalytic mechanisms.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Fu Jiaqi, Li Siying, Guan Hongxin, Li Chuang, Zhao Yan-Bo, Chen Tao-Tao, Xian Wei, Zhang Zhengrui, Liu Yao, Guan Qingtian, Wang Jingting, Lu Qiuhua, Kang Lina, Zheng Si-Ru, Li Jinyu, Cao Shoujing, Das Chittaranjan, Liu Xiaoyun, Song Lei, Ouyang Songying, Luo Zhao-Qing
Аннотация
The intracellular bacterial pathogen Legionella pneumophila modulates host cell functions by secreting multiple effectors with diverse biochemical activities. In particular, effectors of the SidE family interfere with host protein ubiquitination in a process that involves production of phosphoribosyl ubiquitin (PR-Ub). Here, we show that effector LnaB converts PR-Ub into ADP-ribosylated ubiquitin, which is further processed to ADP-ribose and functional ubiquitin by the (ADP-ribosyl)hydrolase MavL, thus maintaining ubiquitin homeostasis in infected cells. Upon being activated by actin, LnaB also undergoes self-AMPylation on tyrosine residues. The activity of LnaB requires a motif consisting of Ser, His and Glu (SHxxxE) present in a large family of toxins from diverse bacterial pathogens. Thus, our study sheds light on the mechanisms by which a pathogen maintains ubiquitin homeostasis and identifies a family of enzymes capable of protein AMPylation.