A Burkholderia type VI effector deamidates Rho GTPases to activate the pyrin inflammasome

Daniel F. Aubert, Hao Xu, Jieling Yang, Xuyan Shi, Wenqing Gao, Lin Li, Fabiana Bisaro, She Chen, Miguel A. Valvano, Feng Shao

Research output: Contribution to journalArticlepeer-review

123 Citations (Scopus)
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Burkholderia cenocepacia is an opportunistic pathogen of the cystic fibrosis lung that elicits a strong inflammatory response. B. cenocepacia employs a type VI secretion system (T6SS) to survive in macrophages by disarming Rho-type GTPases, causing actin cytoskeletal defects. Here, we identified TecA, a non-VgrG T6SS effector responsible for actin disruption. TecA and other bacterial homologs bear a cysteine protease-like catalytic triad, which inactivates Rho GTPases by deamidating a conserved asparagine in the GTPase switch-I region. RhoA deamidation induces caspase-1 inflammasome activation, which is mediated by the familial Mediterranean fever disease protein Pyrin. In mouse infection, the deamidase activity of TecA is necessary and sufficient for B. cenocepacia-triggered lung inflammation and also protects mice from lethal B. cenocepacia infection. Therefore, Burkholderia TecA is a T6SS effector that modifies a eukaryotic target through an asparagine deamidase activity, which in turn elicits host cell death and inflammation through activation of the Pyrin inflammasome.

Original languageEnglish
Pages (from-to)664-674
Number of pages11
JournalCell Host & Microbe
Issue number5
Early online date28 Apr 2016
Publication statusPublished - 11 May 2016


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