Golgi stress induces SIRT2 to counteract Shigella infection via defatty-acylation

Miao Wang, Yugang Zhang, Garrison P. Komaniecki, Xuan Lu, Ji Cao, Mingming Zhang, Tao Yu, Dan Hou, Nicole A. Spiegelman, Ming Yang, Ian R. Price and Hening Lin ()
Additional contact information
Miao Wang: Cornell University
Yugang Zhang: Cornell University
Garrison P. Komaniecki: Cornell University
Xuan Lu: Cornell University
Ji Cao: Cornell University
Mingming Zhang: Cornell University
Tao Yu: Cornell University
Dan Hou: Cornell University
Nicole A. Spiegelman: Cornell University
Ming Yang: Cornell University
Ian R. Price: Cornell University
Hening Lin: Cornell University

Nature Communications, 2022, vol. 13, issue 1, 1-13

Abstract: Abstract Enzymes from pathogens often modulate host protein post-translational modifications (PTMs), facilitating survival and proliferation of pathogens. Shigella virulence factors IpaJ and IcsB induce proteolytic cleavage and lysine fatty acylation on host proteins, which cause Golgi stress and suppress innate immunity, respectively. However, it is unknown whether host enzymes could reverse such modifications introduced by pathogens’ virulence factors to suppress pathogenesis. Herein, we report that SIRT2, a potent lysine defatty-acylase, is upregulated by the transcription factor CREB3 under Golgi stress induced by Shigella infection. SIRT2 in turn removes the lysine fatty acylation introduced by Shigella virulence factor IcsB to enhance host innate immunity. SIRT2 knockout mice are more susceptible to Shigella infection than wildtype mice, demonstrating the importance of SIRT2 to counteract Shigella infection.

Date: 2022
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DOI: 10.1038/s41467-022-32227-x

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