Shigella IpgB1 promotes bacterial entry through the ELMO-Dock180 machinery

Yutaka Handa, Masato Suzuki, Kenji Ohya, Hiroki Iwai, Nozomi Ishijima, Anthony J. Koleske, Yoshinori Fukui, Chihiro Sasakawa

Research output: Contribution to journalArticlepeer-review

125 Citations (Scopus)


Shigella use a special mechanism to invade epithelial cells called 'the trigger mechanism of entry', which allows epithelial cells to trap several bacteria simultaneously. On contact, Shigella deliver effectors into epithelial cells through the type III secretion system. Here, we show that one of the effectors, IpgB1, has a pivotal role in producing membrane ruffles by exploiting the RhoG-ELMO-Dock180 pathway to stimulate Rac1 activity. Using pulldown assays, we identified engulfment and cell motility (ELMO) protein as the IpgB1 binding partner. IpgB1 colocalized with ELMO and Dock180 in membrane ruffles induced by Shigella. Shigella invasiveness and IpgB1-induced ruffles were less in ELMO- and Dock180-knockdown cells compared with wild-type cells. Membrane association of ELMO-Dock180 with ruffles were promoted when cells expressed an IpgB1-ELMO chimera, establishing that IpgB1 mimics the role of RhoG in producing membrane ruffles. Taken together, our findings show that IpgB1 mimicry is the key to invasion by Shigella.

Original languageEnglish
Pages (from-to)121-128
Number of pages8
JournalNature Cell Biology
Issue number1
Publication statusPublished - Jan 2007

All Science Journal Classification (ASJC) codes

  • Cell Biology


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