Journal
NATURE CELL BIOLOGY
Volume 12, Issue 1, Pages 66-U164Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb2006
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Funding
- The Special Coordination Funds for Promoting Science and Technology
- Ministry of Education, Culture, Sports, Science and Technology (MEXT)
- Japan Science and Technology Agency (JST)
- [20229006]
- [20659067]
- [18073003]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK071939] Funding Source: NIH RePORTER
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NF-kappa B (nuclear factor kappa B) has a pivotal role in many cellular processes, including the inflammatory and immune responses and, therefore, its activation is tightly regulated by the IKK (I kappa B kinase) complex and by I kappa B alpha degradation. When Shigella bacteria multiply within epithelial cells they release peptidoglycans, which are recognized by Nod1 and stimulate the NF-kappa B pathway, thus leading to a severe inflammatory response. Here, we show that IpaH9.8, a Shigella effector possessing E3 ligase activity, dampens the NF-kappa B-mediated inflammatory response to the bacterial infection in a unique way. IpaH9.8 interacts with NEMO/IKK gamma and ABIN-1, a ubiquitin-binding adaptor protein, promoting ABIN-1-dependent polyubiquitylation of NEMO. Consequently, polyubiquitylated NEMO undergoes proteasome-dependent degradation, which perturbs NF-kappa B activation. As NEMO is essential for NF-kappa B activation, we propose that the polyubiquitylation and degradation of NEMO during Shigella infection is a new bacterial strategy to modulate host inflammatory responses.
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