RNAi screen reveals a role for PACSIN2 and caveolins during bacterial cell-to-cell spread
Listeria monocytogenes is a human bacterial pathogen that disseminates through host tissues using a process called cell-to-cell spread. This critical yet understudied virulence strategy resembles a vesicular form of intercellular trafficking that allows L. monocytogenes to move between host cells wi...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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American Society for Cell Biology (ASCB)
2020
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| Online Access: | https://hdl.handle.net/1721.1/125523 |
| _version_ | 1811072384664338432 |
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| author | Sanderlin, Allen G Vondrak, Cassandra Scricco, Arianna J. Scricco, Arianna J. Fedrigo, Indro Ahyong, Vida Lamason, Rebecca L. |
| author2 | Massachusetts Institute of Technology. Department of Biology |
| author_facet | Massachusetts Institute of Technology. Department of Biology Sanderlin, Allen G Vondrak, Cassandra Scricco, Arianna J. Scricco, Arianna J. Fedrigo, Indro Ahyong, Vida Lamason, Rebecca L. |
| author_sort | Sanderlin, Allen G |
| collection | MIT |
| description | Listeria monocytogenes is a human bacterial pathogen that disseminates through host tissues using a process called cell-to-cell spread. This critical yet understudied virulence strategy resembles a vesicular form of intercellular trafficking that allows L. monocytogenes to move between host cells without escaping the cell. Interestingly, eukaryotic cells can also directly exchange cellular components via intercellular communication pathways (e.g., trans-endocytosis) using cell–cell adhesion, membrane trafficking, and membrane remodeling proteins. Therefore, we hypothesized that L. monocytogenes would hijack these types of host proteins during spread. Using a focused RNA interference screen, we identified 22 host genes that are important for L. monocytogenes spread. We then found that caveolins (CAV1 and CAV2) and the membrane sculpting F-BAR protein PACSIN2 promote L. monocytogenes protrusion engulfment during spread, and that PACSIN2 specifically localizes to protrusions. Overall, our study demonstrates that host intercellular communication pathways may be coopted during bacterial spread and that specific trafficking and membrane remodeling proteins promote bacterial protrusion resolution. |
| first_indexed | 2024-09-23T09:05:14Z |
| format | Article |
| id | mit-1721.1/125523 |
| institution | Massachusetts Institute of Technology |
| language | English |
| last_indexed | 2024-09-23T09:05:14Z |
| publishDate | 2020 |
| publisher | American Society for Cell Biology (ASCB) |
| record_format | dspace |
| spelling | mit-1721.1/1255232022-09-26T10:21:38Z RNAi screen reveals a role for PACSIN2 and caveolins during bacterial cell-to-cell spread Sanderlin, Allen G Vondrak, Cassandra Scricco, Arianna J. Scricco, Arianna J. Fedrigo, Indro Ahyong, Vida Lamason, Rebecca L. Massachusetts Institute of Technology. Department of Biology Listeria monocytogenes is a human bacterial pathogen that disseminates through host tissues using a process called cell-to-cell spread. This critical yet understudied virulence strategy resembles a vesicular form of intercellular trafficking that allows L. monocytogenes to move between host cells without escaping the cell. Interestingly, eukaryotic cells can also directly exchange cellular components via intercellular communication pathways (e.g., trans-endocytosis) using cell–cell adhesion, membrane trafficking, and membrane remodeling proteins. Therefore, we hypothesized that L. monocytogenes would hijack these types of host proteins during spread. Using a focused RNA interference screen, we identified 22 host genes that are important for L. monocytogenes spread. We then found that caveolins (CAV1 and CAV2) and the membrane sculpting F-BAR protein PACSIN2 promote L. monocytogenes protrusion engulfment during spread, and that PACSIN2 specifically localizes to protrusions. Overall, our study demonstrates that host intercellular communication pathways may be coopted during bacterial spread and that specific trafficking and membrane remodeling proteins promote bacterial protrusion resolution. National Institutes of Health (Grant S10OD-021828) National Institutes of Health (Grant T32GM-007287) National Institutes of Health (Grant R00GM-115765) 2020-05-27T19:48:04Z 2020-05-27T19:48:04Z 2019-08 2019-06 2020-04-24T12:49:33Z Article http://purl.org/eprint/type/JournalArticle 1059-1524 1939-4586 https://hdl.handle.net/1721.1/125523 Sanderlin, Allen G. et al. "RNAi screen reveals a role for PACSIN2 and caveolins during bacterial cell-to-cell spread." Molecular Biology of the Cell 30, 17 (August 2019): 2097-2347 © 2019 The Author(s) en http://dx.doi.org/10.1091/mbc.e19-04-0197 Molecular Biology of the Cell Creative Commons Attribution Noncommercial 3.0 unported license https://creativecommons.org/licenses/by-nc/3.0/ application/pdf American Society for Cell Biology (ASCB) American Society for Cell Biology |
| spellingShingle | Sanderlin, Allen G Vondrak, Cassandra Scricco, Arianna J. Scricco, Arianna J. Fedrigo, Indro Ahyong, Vida Lamason, Rebecca L. RNAi screen reveals a role for PACSIN2 and caveolins during bacterial cell-to-cell spread |
| title | RNAi screen reveals a role for PACSIN2 and caveolins during bacterial cell-to-cell spread |
| title_full | RNAi screen reveals a role for PACSIN2 and caveolins during bacterial cell-to-cell spread |
| title_fullStr | RNAi screen reveals a role for PACSIN2 and caveolins during bacterial cell-to-cell spread |
| title_full_unstemmed | RNAi screen reveals a role for PACSIN2 and caveolins during bacterial cell-to-cell spread |
| title_short | RNAi screen reveals a role for PACSIN2 and caveolins during bacterial cell-to-cell spread |
| title_sort | rnai screen reveals a role for pacsin2 and caveolins during bacterial cell to cell spread |
| url | https://hdl.handle.net/1721.1/125523 |
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