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NBR1 acts as an autophagy receptor for peroxisomes

Deosaran, Elizabeth, Larsen, Kenneth B., Hua, Rong, Sargent, Graeme, Wang, Yuqing, Kim, Sarah, Lamark, Trond, Jauregui, Miluska, Law, Kelsey, Lippincott-Schwartz, Jennifer, Brech, Andreas, Johansen, Terje, Kim, Peter K.·2012·Journal of Cell Science

Abstract

Selective macro-autophagy is an intracellular process by which large cytoplasmic materials are selectively sequestered and degraded in the lysosomes. Substrate selection is mediated by ubiquitination and recruitment of ubiquitin-binding autophagic receptors such as p62, NBR1, NDP52 and Optineurin. Although it has been shown that these receptors act cooperatively to target some types of substrates to nascent autophagosomes, their precise roles are not well understood. Here, we examined selective autophagic degradation of peroxisomes (pexophagy), and found that NBR1 is necessary and sufficient for pexophagy. Mutagenesis studies of NBR1 showed that the amphipathic α-helical J domain, the ubiquitin-associated (UBA) domain, the LC3 interacting region and the coiled-coil domain are necessary to mediate pexophagy. Strikingly, substrate selectivity is partly achieved by NBR1 itself by coincident binding of the J and UBA domains to peroxisomes. Although p62 is not required when NBR1 is in excess, its binding to NBR1 increases the efficiency of NBR1 mediated pexophagy. Together, these results suggest that NBR1 is the specific autophagy receptor for pexophagy.

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Research works printed but not linked: 34

  1. Bjørkøy, 2005, p62/SQSTM1 forms protein aggregates degraded by autophagy and has a protective effect on huntingtin-induced cell death., J. Cell Biol., 171, 603, 10.1083/jcb.200507002 · DOI · Paper page
  2. Bolte, 2006, A guided tour into subcellular colocalization analysis in light microscopy., J. Microsc., 224, 213, 10.1111/j.1365-2818.2006.01706.x · DOI
  3. Carlton, 2005, Coincidence detection in phosphoinositide signaling., Trends Cell Biol., 15, 540, 10.1016/j.tcb.2005.08.005 · DOI
  4. Cemma, 2011, The ubiquitin-binding adaptor proteins p62/SQSTM1 and NDP52 are recruited independently to bacteria-associated microdomains to target Salmonella to the autophagy pathway., Autophagy, 7, 341, 10.4161/auto.7.3.14046 · DOI
  5. Ding, 2010, Nix is critical to two distinct phases of mitophagy, reactive oxygen species-mediated autophagy induction and Parkin-ubiquitin-p62-mediated mitochondrial priming., J. Biol. Chem., 285, 27879, 10.1074/jbc.M110.119537 · DOI · Paper page
  6. Hara–Kuge, 2008, The peroxin Pex14p is involved in LC3-dependent degradation of mammalian peroxisomes., Exp. Cell Res., 314, 3531, 10.1016/j.yexcr.2008.09.015 · DOI
  7. Huang, 2011, Antibacterial autophagy occurs at PI(3)P-enriched domains of the endoplasmic reticulum and requires Rab1 GTPase., Autophagy, 7, 17, 10.4161/auto.7.1.13840 · DOI
  8. Itakura, 2011, p62 Targeting to the autophagosome formation site requires self-oligomerization but not LC3 binding., J. Cell Biol., 192, 17, 10.1083/jcb.201009067 · DOI
  9. Iwata, 2006, Excess peroxisomes are degraded by autophagic machinery in mammals., J. Biol. Chem., 281, 4035, 10.1074/jbc.M512283200 · DOI · Paper page
  10. Johansen, 2011, Selective autophagy mediated by autophagic adapter proteins., Autophagy, 7, 279, 10.4161/auto.7.3.14487 · DOI
  11. Kassmann, 2008, Oligodendroglial impact on axonal function and survival – a hypothesis., Curr. Opin. Neurol., 21, 235, 10.1097/WCO.0b013e328300c71f · DOI
  12. Kim, 2008, Ubiquitin signals autophagic degradation of cytosolic proteins and peroxisomes., Proc. Natl. Acad. Sci. USA, 105, 20567, 10.1073/pnas.0810611105 · DOI
  13. Kirkin, 2009, A role for NBR1 in autophagosomal degradation of ubiquitinated substrates., Mol. Cell, 33, 505, 10.1016/j.molcel.2009.01.020 · DOI · Paper page
  14. Kirkin, 2009, A role for ubiquitin in selective autophagy., Mol. Cell, 34, 259, 10.1016/j.molcel.2009.04.026 · DOI
  15. Komatsu, 2010, Selective autophagy regulates various cellular functions., Genes Cells, 15, 923, 10.1111/j.1365-2443.2010.01433.x · DOI
  16. Kraft, 2010, Selective autophagy: ubiquitin-mediated recognition and beyond., Nat. Cell Biol., 12, 836, 10.1038/ncb0910-836 · DOI · Paper page
  17. Kutateladze, 2006, Phosphatidylinositol 3-phosphate recognition and membrane docking by the FYVE domain., Biochim. Biophys. Acta, 1761, 868, 10.1016/j.bbalip.2006.03.011 · DOI
  18. Lamark, 2003, Interaction codes within the family of mammalian Phox and Bem1p domain-containing proteins., J. Biol. Chem., 278, 34568, 10.1074/jbc.M303221200 · DOI
  19. Mardakheh, 2010, Nbr1 is a novel inhibitor of ligand-mediated receptor tyrosine kinase degradation., Mol. Cell. Biol., 30, 5672, 10.1128/MCB.00878-10 · DOI
  20. Meinecke, 2010, The peroxisomal importomer constitutes a large and highly dynamic pore., Nat. Cell Biol., 12, 273, 10.1038/ncb2027 · DOI
  21. Mitra, 2009, A hyperfused mitochondrial state achieved at G1-S regulates cyclin E buildup and entry into S phase., Proc. Natl. Acad. Sci. USA, 106, 11960, 10.1073/pnas.0904875106 · DOI
  22. Motley, 2012, Pex3-anchored Atg36 tags peroxisomes for degradation in Saccharomyces cerevisiae., EMBO J., 31, 2852, 10.1038/emboj.2012.151 · DOI
  23. Narendra, 2010, p62/SQSTM1 is required for Parkin-induced mitochondrial clustering but not mitophagy; VDAC1 is dispensable for both., Autophagy, 6, 1090, 10.4161/auto.6.8.13426 · DOI
  24. Platta, 2007, Peroxisomal dynamics., Trends Cell Biol., 17, 474, 10.1016/j.tcb.2007.06.009 · DOI
  25. Platta, 2007, Ubiquitination of the peroxisomal import receptor Pex5p is required for its recycling., J. Cell Biol., 177, 197, 10.1083/jcb.200611012 · DOI
  26. Rambold, 2011, Tubular network formation protects mitochondria from autophagosomal degradation during nutrient starvation., Proc. Natl. Acad. Sci. USA, 108, 10190, 10.1073/pnas.1107402108 · DOI
  27. Ribeiro, 2012, Peroxisome morphology in pathology., Histol. Histopathol., 27, 661
  28. Rizzo, 2004, An improved cyan fluorescent protein variant useful for FRET., Nat. Biotechnol., 22, 445, 10.1038/nbt945 · DOI
  29. Singh, 2009, Peroxisomal dysfunction in inflammatory childhood white matter disorders: an unexpected contributor to neuropathology., J. Child Neurol., 24, 1147, 10.1177/0883073809338327 · DOI
  30. Thurston, 2009, The TBK1 adaptor and autophagy receptor NDP52 restricts the proliferation of ubiquitin-coated bacteria., Nat. Immunol., 10, 1215, 10.1038/ni.1800 · DOI
  31. Till, 2012, Pexophagy: the selective degradation of peroxisomes., Int. J. Cell Biol., 2012, 512721, 10.1155/2012/512721 · DOI
  32. Wild, 2011, Phosphorylation of the autophagy receptor optineurin restricts Salmonella growth., Science, 333, 228, 10.1126/science.1205405 · DOI · Paper page
  33. Wilson, 2003, PB1 domain-mediated heterodimerization in NADPH oxidase and signaling complexes of atypical protein kinase C with Par6 and p62., Mol. Cell, 12, 39, 10.1016/S1097-2765(03)00246-6 · DOI
  34. Zheng, 2009, The adaptor protein p62/SQSTM1 targets invading bacteria to the autophagy pathway., J. Immunol., 183, 5909, 10.4049/jimmunol.0900441 · DOI

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Metadata

Authors
Deosaran, E., Larsen, K. B., Hua, R., Sargent, G., Wang, Y., Kim, S., Lamark, T., Jauregui, M., Law, K., Lippincott-Schwartz, J., Brech, A., Johansen, T., & Kim, P. K.
Venue
Journal of Cell Science
Published
2012-01-01
ISSN
  • 1477-9137
  • 0021-9533
Cited by
232
References
7
Language
en

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CoChat. (2026). Citation check: NBR1 acts as an autophagy receptor for peroxisomes. https://app.cochat.ai/papers/10.1242/jcs.114819
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Deosaran, E., Larsen, K. B., Hua, R., Sargent, G., Wang, Y., Kim, S., Lamark, T., Jauregui, M., Law, K., Lippincott-Schwartz, J., Brech, A., Johansen, T., & Kim, P. K. (2012). NBR1 acts as an autophagy receptor for peroxisomes. Journal of Cell Science. https://doi.org/10.1242/jcs.114819