Shigella entry unveils a calcium/calpain-dependent mechanism for inhibiting sumoylation

Pierre Lapaquette, Sabrina Fritah, Nouara Lhocine, Alexandra Andrieux, Giulia Nigro, Joëlle Mounier, Philippe Sansonetti*, Anne Dejean

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

13 Citations (Scopus)


Disruption of the sumoylation/desumoylation equilibrium is associated with several disease states such as cancer and infections, however the mechanisms regulating the global SUMO balance remain poorly defined. Here, we show that infection by Shigella flexneri, the causative agent of human bacillary dysentery, switches off host sumoylation during epithelial cell infection in vitro and in vivo and that this effect is mainly mediated by a calcium/calpain-induced cleavage of the SUMO E1 enzyme SAE2, thus leading to sumoylation inhibition. Furthermore, we describe a mechanism by which Shigella promotes its own invasion by altering the sumoylation state of RhoGDIα, a master negative regulator of RhoGTPase activity and actin polymerization. Together, our data suggest that SUMO modification is essential to restrain pathogenic bacterial entry by limiting cytoskeletal rearrangement induced by bacterial effectors. Moreover, these findings identify calcium-activated calpains as powerful modulators of cellular sumoylation levels with potentially broad implications in several physiological and pathological situations.

Original languageEnglish
Article numbere27444
Publication statusPublished - 12 Dec 2017


Dive into the research topics of 'Shigella entry unveils a calcium/calpain-dependent mechanism for inhibiting sumoylation'. Together they form a unique fingerprint.

Cite this