Journal ArticleDOI
Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry
Leonardo H. Travassos,Leticia A.M. Carneiro,Mahendrasingh Ramjeet,Seamus Hussey,Seamus Hussey,Yun Gi Kim,Joao G. Magalhaes,Linda Yuan,Fraser Soares,Evelyn Chea,Lionel Le Bourhis,Ivo G Boneca,Abdelmounaaim Allaoui,Nicola L. Jones,Gabriel Núñez,Stephen E. Girardin,Dana J. Philpott +16 more
TLDR
The results link bacterial sensing by Nod proteins to the induction of autophagy and provide a functional link between Nod2 and ATG16L1, which are encoded by two of the most important genes associated with Crohn's disease.Abstract:
Autophagy is emerging as a crucial defense mechanism against bacteria, but the host intracellular sensors responsible for inducing autophagy in response to bacterial infection remain unknown. Here we demonstrated that the intracellular sensors Nod1 and Nod2 are critical for the autophagic response to invasive bacteria. By a mechanism independent of the adaptor RIP2 and transcription factor NF-kappaB, Nod1 and Nod2 recruited the autophagy protein ATG16L1 to the plasma membrane at the bacterial entry site. In cells homozygous for the Crohn's disease-associated NOD2 frameshift mutation, mutant Nod2 failed to recruit ATG16L1 to the plasma membrane and wrapping of invading bacteria by autophagosomes was impaired. Our results link bacterial sensing by Nod proteins to the induction of autophagy and provide a functional link between Nod2 and ATG16L1, which are encoded by two of the most important genes associated with Crohn's disease.read more
Citations
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Journal ArticleDOI
Autophagy in PDGFRα+ mesenchymal cells is essential for intestinal stem cell survival
Yang Yang,Maria Macarena Gomez,Timothy Marsh,Laura Poillet-Perez,Akshada Sawant,Lei Chen,Noel R. Park,S. RaElle Jackson,Zhixiang Hu,Noga Alon,Chen Liu,Jayanta Debnath,Jun-Lin Guan,Shawn M. Davidson,Michael P. Verzi,Eileen White +15 more
TL;DR: It is shown that conditional whole-body deletion of Atg5 or Fip200, but not Atg7, is lethal due to loss of ileum stem cells and barrier function likely caused by different kinetics of autophagy loss, which was rescued by slow deletion.
Journal ArticleDOI
Evidence and speculation: the response of Salmonella confronted by autophagy in macrophages
TL;DR: Novel findings onSalmonella and macrophage autophagy as a mechanism against infection are introduced and the strategies used by Salmonella to escape autophagosomes are explored.
Journal ArticleDOI
Different modalities of host cell death and their impact on Mycobacterium tuberculosis infection.
Annuurun Nisa,Franciele Cristina Kipper,Dipak Panigrahy,Sangeeta Tiwari,Andreas Kupz,Selvakumar Subbian +5 more
TL;DR: Different modalities of Mtb-mediated host cell deaths, the molecular mechanisms underpinning the host cell death during Mtb infection, and its potential implications for host immunity are summarized.
Book ChapterDOI
Lysosome Biogenesis and Autophagy
TL;DR: This chapter presents an overview of these two major degradative intracellular pathways, and highlights the emerging cross talks between them, in healthy and diseased conditions.
Journal ArticleDOI
Exploring the hidden heritability of inflammatory bowel disease
TL;DR: Evidence is provided that Crohn's disease and ulcerative colitis are related complex diseases, sharing some, but not all, susceptibility loci, and many of the genetic determinants involved in IBD are also implicated in other complex disorders, such as type I diabetes and coeliac disease.
References
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Autophagy fights disease through cellular self-digestion
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Journal ArticleDOI
Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease
Jean-Pierre Hugot,Mathias Chamaillard,Mathias Chamaillard,Habib Zouali,Suzanne Lesage,Jean-Pierre Cézard,Jacques Belaiche,Sven Almer,Curt Tysk,Colm O'Morain,Miquel A. Gassull,Vibeke Binder,Yigael Finkel,Antoine Cortot,Robert Modigliani,Pierre Laurent-Puig,C. Gower-Rousseau,J. Macry,Jean-Frederic Colombel,Mourad Sahbatou,Gilles Thomas,Gilles Thomas +21 more
TL;DR: It is suggested that the NOD2 gene product confers susceptibility to Crohn's disease by altering the recognition of these components and/or by over-activating NF-kB in monocytes, thus documenting a molecular model for the pathogenic mechanism of Crohn’s disease that can now be further investigated.
Journal ArticleDOI
Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice
Taichi Hara,Kenji Nakamura,Makoto Matsui,Makoto Matsui,Makoto Matsui,Akitsugu Yamamoto,Yohko Nakahara,Rika Suzuki-Migishima,Minesuke Yokoyama,Kenji Mishima,Ichiro Saito,Hideyuki Okano,Noboru Mizushima +12 more
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Journal ArticleDOI
Nod2 is a general sensor of peptidoglycan through muramyl dipeptide (MDP) detection.
Stephen E. Girardin,Ivo G. Boneca,Jérôme Viala,Mathias Chamaillard,Agnès Labigne,Gilles Thomas,Dana J. Philpott,Philippe J. Sansonetti +7 more
TL;DR: It is shown here that Nod2 is a general sensor of peptidoglycan through the recognition of muramyl dipeptide (MDP), the minimal bioactive peptIDoglycan motif common to all bacteria.
Journal ArticleDOI
Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes
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TL;DR: A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.
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