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HIV-1 Nef Binds a Subpopulation of MHC-I throughout Its Trafficking Itinerary and Down-regulates MHC-I by Perturbing Both Anterograde and Retrograde Trafficking
The HIV protein Nef is thought to mediate immune evasion and promote viral persistence in part by down-regulating major histocompatibility complex class I protein (MHC-I or HLA-I) from the cell surface. Two different models have been proposed to explain this phenomenon as follows: 1) stimulation of...
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Published in: | The Journal of biological chemistry 2010-10, Vol.285 (40), p.30884-30905 |
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description | The HIV protein Nef is thought to mediate immune evasion and promote viral persistence in part by down-regulating major histocompatibility complex class I protein (MHC-I or HLA-I) from the cell surface. Two different models have been proposed to explain this phenomenon as follows: 1) stimulation of MHC-I retrograde trafficking from and aberrant recycling to the plasma membrane, and 2) inhibition of anterograde trafficking of newly synthesized HLA-I from the endoplasmic reticulum to the plasma membrane. We show here that Nef simultaneously uses both mechanisms to down-regulate HLA-I in peripheral blood mononuclear cells or HeLa cells. Consistent with this, we found by using fluorescence correlation spectroscopy that a third of diffusing HLA-I at the endoplasmic reticulum, Golgi/trans-Golgi network, and the plasma membrane (PM) was associated with Nef. The binding of Nef was similarly avid for native HLA-I and recombinant HLA-I A2 at the PM. Nef binding to HLA-I at the PM was sensitive to specific inhibition of endocytosis. It was also attenuated by cyclodextrin disruption of PM lipid micro-domain architecture, a change that also retarded lateral diffusion and induced large clusters of HLA-I. In all, our data support a model for Nef down-regulation of HLA-I that involves both major trafficking itineraries and persistent protein-protein interactions throughout the cell. |
doi_str_mv | 10.1074/jbc.M110.135947 |
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Two different models have been proposed to explain this phenomenon as follows: 1) stimulation of MHC-I retrograde trafficking from and aberrant recycling to the plasma membrane, and 2) inhibition of anterograde trafficking of newly synthesized HLA-I from the endoplasmic reticulum to the plasma membrane. We show here that Nef simultaneously uses both mechanisms to down-regulate HLA-I in peripheral blood mononuclear cells or HeLa cells. Consistent with this, we found by using fluorescence correlation spectroscopy that a third of diffusing HLA-I at the endoplasmic reticulum, Golgi/trans-Golgi network, and the plasma membrane (PM) was associated with Nef. The binding of Nef was similarly avid for native HLA-I and recombinant HLA-I A2 at the PM. Nef binding to HLA-I at the PM was sensitive to specific inhibition of endocytosis. It was also attenuated by cyclodextrin disruption of PM lipid micro-domain architecture, a change that also retarded lateral diffusion and induced large clusters of HLA-I. In all, our data support a model for Nef down-regulation of HLA-I that involves both major trafficking itineraries and persistent protein-protein interactions throughout the cell.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M110.135947</identifier><identifier>PMID: 20622010</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adapter Proteins ; Anterograde transport ; Cell Biology ; Cell Membrane - genetics ; Cell Membrane - metabolism ; Cell surface ; Cell Surface Receptor ; cyclodextrin ; Data processing ; Endocytosis ; Endocytosis - genetics ; Endoplasmic reticulum ; Endoplasmic Reticulum - genetics ; Endoplasmic Reticulum - metabolism ; FCS ; fluorescence spectroscopy ; FRAP ; Golgi apparatus ; Golgi Apparatus - genetics ; Golgi Apparatus - metabolism ; HeLa Cells ; Histocompatibility ; Histocompatibility antigen HLA ; Histocompatibility Antigens Class I - genetics ; Histocompatibility Antigens Class I - metabolism ; HIV-1 - genetics ; HIV-1 - metabolism ; Human Immunodeficiency Virus ; Human immunodeficiency virus 1 ; Humans ; Immunology ; Lateral diffusion ; Leukocytes, Mononuclear - metabolism ; Leukocytes, Mononuclear - virology ; Lipids ; Major histocompatibility complex ; Models, Biological ; nef Gene Products, Human Immunodeficiency Virus - genetics ; nef Gene Products, Human Immunodeficiency Virus - metabolism ; Nef protein ; Peripheral blood mononuclear cells ; Plasma membranes ; Protein interaction ; Protein Sorting ; Protein Transport ; Recycling ; Retrograde transport</subject><ispartof>The Journal of biological chemistry, 2010-10, Vol.285 (40), p.30884-30905</ispartof><rights>2010 © 2010 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><rights>2010 by The American Society for Biochemistry and Molecular Biology, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c572t-9cabcf119e8c7ac2cca4c66992aca5b6fa32b69e2c10d3ab2ee9d7e97fa302b33</citedby><cites>FETCH-LOGICAL-c572t-9cabcf119e8c7ac2cca4c66992aca5b6fa32b69e2c10d3ab2ee9d7e97fa302b33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2945581/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0021925819889780$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,3536,27905,27906,45761,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20622010$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yi, Ling</creatorcontrib><creatorcontrib>Rosales, Tilman</creatorcontrib><creatorcontrib>Rose, Jeremy J.</creatorcontrib><creatorcontrib>Chaudhury, Bhabhadeb</creatorcontrib><creatorcontrib>Knutson, Jay R.</creatorcontrib><creatorcontrib>Venkatesan, Sundararajan</creatorcontrib><title>HIV-1 Nef Binds a Subpopulation of MHC-I throughout Its Trafficking Itinerary and Down-regulates MHC-I by Perturbing Both Anterograde and Retrograde Trafficking</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>The HIV protein Nef is thought to mediate immune evasion and promote viral persistence in part by down-regulating major histocompatibility complex class I protein (MHC-I or HLA-I) from the cell surface. Two different models have been proposed to explain this phenomenon as follows: 1) stimulation of MHC-I retrograde trafficking from and aberrant recycling to the plasma membrane, and 2) inhibition of anterograde trafficking of newly synthesized HLA-I from the endoplasmic reticulum to the plasma membrane. We show here that Nef simultaneously uses both mechanisms to down-regulate HLA-I in peripheral blood mononuclear cells or HeLa cells. Consistent with this, we found by using fluorescence correlation spectroscopy that a third of diffusing HLA-I at the endoplasmic reticulum, Golgi/trans-Golgi network, and the plasma membrane (PM) was associated with Nef. The binding of Nef was similarly avid for native HLA-I and recombinant HLA-I A2 at the PM. Nef binding to HLA-I at the PM was sensitive to specific inhibition of endocytosis. It was also attenuated by cyclodextrin disruption of PM lipid micro-domain architecture, a change that also retarded lateral diffusion and induced large clusters of HLA-I. In all, our data support a model for Nef down-regulation of HLA-I that involves both major trafficking itineraries and persistent protein-protein interactions throughout the cell.</description><subject>Adapter Proteins</subject><subject>Anterograde transport</subject><subject>Cell Biology</subject><subject>Cell Membrane - genetics</subject><subject>Cell Membrane - metabolism</subject><subject>Cell surface</subject><subject>Cell Surface Receptor</subject><subject>cyclodextrin</subject><subject>Data processing</subject><subject>Endocytosis</subject><subject>Endocytosis - genetics</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum - genetics</subject><subject>Endoplasmic Reticulum - metabolism</subject><subject>FCS</subject><subject>fluorescence spectroscopy</subject><subject>FRAP</subject><subject>Golgi apparatus</subject><subject>Golgi Apparatus - genetics</subject><subject>Golgi Apparatus - metabolism</subject><subject>HeLa Cells</subject><subject>Histocompatibility</subject><subject>Histocompatibility antigen HLA</subject><subject>Histocompatibility Antigens Class I - genetics</subject><subject>Histocompatibility Antigens Class I - metabolism</subject><subject>HIV-1 - genetics</subject><subject>HIV-1 - metabolism</subject><subject>Human Immunodeficiency Virus</subject><subject>Human immunodeficiency virus 1</subject><subject>Humans</subject><subject>Immunology</subject><subject>Lateral diffusion</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Leukocytes, Mononuclear - virology</subject><subject>Lipids</subject><subject>Major histocompatibility complex</subject><subject>Models, Biological</subject><subject>nef Gene Products, Human Immunodeficiency Virus - genetics</subject><subject>nef Gene Products, Human Immunodeficiency Virus - metabolism</subject><subject>Nef protein</subject><subject>Peripheral blood mononuclear cells</subject><subject>Plasma membranes</subject><subject>Protein interaction</subject><subject>Protein Sorting</subject><subject>Protein Transport</subject><subject>Recycling</subject><subject>Retrograde transport</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNqFkk9v1DAQxSMEokvhzA35ximt7cRxfEFqlz-7UgsICuJm2c5k1yVrb22nqN-Gj4rDbqtyQPXFGs3vPc3YryheEnxEMK-PL7U5OidTVTFR80fFjOC2KitGfjwuZhhTUgrK2oPiWYyXOJ9akKfFAcUNpZjgWfF7sfxeEvQRenRqXReRQl9HvfXbcVDJeod8j84X83KJ0jr4cbX2Y0LLFNFFUH1vzU_rVrm2DoIKN0i5Dr31v1wZYDU5QNyr9Q36DCGNQU-CU5_W6MQlCH4VVAd_dV8g3Zb3zJ8XT3o1RHixvw-Lb-_fXcwX5dmnD8v5yVlpGKepFEZp0xMioDVcGWqMqk3TCEGVUUw3vaqobgRQQ3BXKU0BRMdB8NzAVFfVYfFm57sd9QY6Ay4FNchtsJu8mPTKyn87zq7lyl9LKmrGWpINXu8Ngr8aISa5sdHAMCgHfoyy5TXhgjXVgyTPn9PituUPk4zVmDAsMnm8I03wMQbo7yYnWE5RkTkqcoqK3EUlK17dX_iOv81GBsQOgPzs1xaCjMaCM9DZACbJztv_mv8B4ynQSQ</recordid><startdate>20101001</startdate><enddate>20101001</enddate><creator>Yi, Ling</creator><creator>Rosales, Tilman</creator><creator>Rose, Jeremy J.</creator><creator>Chaudhury, Bhabhadeb</creator><creator>Knutson, Jay R.</creator><creator>Venkatesan, Sundararajan</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20101001</creationdate><title>HIV-1 Nef Binds a Subpopulation of MHC-I throughout Its Trafficking Itinerary and Down-regulates MHC-I by Perturbing Both Anterograde and Retrograde Trafficking</title><author>Yi, Ling ; 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Two different models have been proposed to explain this phenomenon as follows: 1) stimulation of MHC-I retrograde trafficking from and aberrant recycling to the plasma membrane, and 2) inhibition of anterograde trafficking of newly synthesized HLA-I from the endoplasmic reticulum to the plasma membrane. We show here that Nef simultaneously uses both mechanisms to down-regulate HLA-I in peripheral blood mononuclear cells or HeLa cells. Consistent with this, we found by using fluorescence correlation spectroscopy that a third of diffusing HLA-I at the endoplasmic reticulum, Golgi/trans-Golgi network, and the plasma membrane (PM) was associated with Nef. The binding of Nef was similarly avid for native HLA-I and recombinant HLA-I A2 at the PM. Nef binding to HLA-I at the PM was sensitive to specific inhibition of endocytosis. It was also attenuated by cyclodextrin disruption of PM lipid micro-domain architecture, a change that also retarded lateral diffusion and induced large clusters of HLA-I. In all, our data support a model for Nef down-regulation of HLA-I that involves both major trafficking itineraries and persistent protein-protein interactions throughout the cell.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>20622010</pmid><doi>10.1074/jbc.M110.135947</doi><tpages>22</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adapter Proteins Anterograde transport Cell Biology Cell Membrane - genetics Cell Membrane - metabolism Cell surface Cell Surface Receptor cyclodextrin Data processing Endocytosis Endocytosis - genetics Endoplasmic reticulum Endoplasmic Reticulum - genetics Endoplasmic Reticulum - metabolism FCS fluorescence spectroscopy FRAP Golgi apparatus Golgi Apparatus - genetics Golgi Apparatus - metabolism HeLa Cells Histocompatibility Histocompatibility antigen HLA Histocompatibility Antigens Class I - genetics Histocompatibility Antigens Class I - metabolism HIV-1 - genetics HIV-1 - metabolism Human Immunodeficiency Virus Human immunodeficiency virus 1 Humans Immunology Lateral diffusion Leukocytes, Mononuclear - metabolism Leukocytes, Mononuclear - virology Lipids Major histocompatibility complex Models, Biological nef Gene Products, Human Immunodeficiency Virus - genetics nef Gene Products, Human Immunodeficiency Virus - metabolism Nef protein Peripheral blood mononuclear cells Plasma membranes Protein interaction Protein Sorting Protein Transport Recycling Retrograde transport |
title | HIV-1 Nef Binds a Subpopulation of MHC-I throughout Its Trafficking Itinerary and Down-regulates MHC-I by Perturbing Both Anterograde and Retrograde Trafficking |
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