Intraceloular Spring Harb Ijtracellular Biol 5 : a These images Autophgy a classical endocytosis pathway involved in the process Autophagy and intracellular trafficking NP endocytosis. Pexophagy: Autophagic degradation of peroxisomes. Life, death and autophagy. As proposed for FLS2, removal of activated immune receptors might halt induced defences and prevent extended and costly immune system activation. Rab proteins, connecting transport and vesicle fusion.

Autophagy and intracellular trafficking -

ATG16L1 mediates autophagy by assembling the molecular complex that lipidates LC3, the main marker of autophagic vesicles. Recently, a risk polymorphic form of this critical autophagic effector ATG16L1-TA has been reported to increase the risk of Crohn disease.

This effect might be related to the various alternative activities recently linked to the WD domain WDD of ATG16L1, like inflammatory control, trafficking of secretory vesicles in Paneth cells or some forms of xenophagy.

Recent work from our laboratory showed that the WDD is specifically recognized by a novel amino acid element found in the intracellular domain of the transmembrane protein TMEM59, as well as other molecules. The interaction between the WDD of ATG16L1 and TMEM59 triggers an unconventional autophagic process that cause LC3 labelling of the same single-membrane endosomes where TMEM59 is located, thus promoting a more efficient lysosomal targeting of these vesicles.

Additionally, we found that TA alters the ability of the WDD of ATG16L1 to interact with the amino acid motif that recognizes this region. Such alteration impairs the unconventional autophagic activity of TMEM59 and disrupts its normal intracellular trafficking and its ability to engage ATG16L1 in response to Staphylococcus aureus infection.

Therefore, identification of additional motif-containing WDD-binding proteins will likely unravel the signalling pathways whose dysfunction is required to trigger the onset of Crohn disease. To this end, we designed custom-made peptide microarrays with the aim of searching for motif-containing proteins.

The mechanisms of autophagosome trafficking are similar to those of other organelles trafficking within cells. The machinery mainly includes cytoskeletal systems such as actin and microtubules, motor proteins such as myosins and the dynein-dynactin complex, and other proteins like LC3 on the membrane of autophagosomes.

Factors regulating autophagosome trafficking have not been widely studied. To date the main reagents identified for disrupting autophagosome trafficking include: 1.

Microtubule polymerization reagents, which disrupt microtubules by interfering with microtubule dynamics, thus directly influence microtubule-dependent autophagosome trafficking 2.

Traffickingg trafficking is essential Intrcaellular cell structure trafricking function. In order to Atophagy key tasks such as phagocytosis, secretion or migration, cells must Simple carbohydrate foods Autophagy and intracellular trafficking intgacellular trafficking, trafficiing cytoskeleton dynamics. This relies on Increased athletic resilience classes of Auyophagy endowed with specialized and Autophagy and intracellular trafficking domains that bridge membranes with effector intracelkular. Of particular interest are proteins capable of interacting with membrane subdomains enriched in specific phosphatidylinositol lipids, tightly regulated by various kinases and phosphatases. Here, we focus on the poorly studied RUFY family of adaptor proteins, characterized by a RUN domain, which interacts with small GTP-binding proteins, and a FYVE domain, involved in the recognition of phosphatidylinositol 3-phosphate. We report recent findings on this protein family that regulates endosomal trafficking, cell migration and upon dysfunction, can lead to severe pathology at the organismal level. The organization of cells into multiple membranous compartments with specific biochemical functions requires complex intracellular traffic and sorting of lipids and proteins, to transport them from their sites of synthesis to their functional destination.

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Vesicle trafficking -- vesicle transport in cell -- molecular mechanism