The Wolbachia WalE1 effector alters Drosophila endocytosis.
The most common intracellular bacterial infection is Wolbachia pipientis, a microbe that manipulates host reproduction and is used in control of insect vectors. Phenotypes induced by Wolbachia have been studied for decades and range from sperm-egg incompatibility to male killing. How Wolbachia alter...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2024-03-01
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| Series: | PLoS Pathogens |
| Online Access: | https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1011245&type=printable |
| _version_ | 1797213313398996992 |
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| author | MaryAnn Martin Sergio López-Madrigal Irene L G Newton |
| author_facet | MaryAnn Martin Sergio López-Madrigal Irene L G Newton |
| author_sort | MaryAnn Martin |
| collection | DOAJ |
| description | The most common intracellular bacterial infection is Wolbachia pipientis, a microbe that manipulates host reproduction and is used in control of insect vectors. Phenotypes induced by Wolbachia have been studied for decades and range from sperm-egg incompatibility to male killing. How Wolbachia alters host biology is less well understood. Previously, we characterized the first Wolbachia effector-WalE1, which encodes an alpha-synuclein domain at the N terminus. Purified WalE1 sediments with and bundles actin and when heterologously expressed in flies, increases Wolbachia titer in the developing oocyte. In this work, we first identify the native expression of WalE1 by Wolbachia infecting both fly cells and whole animals. WalE1 appears as aggregates in the host cell cytosol. We next show that WalE1 co-immunoprecipitates with the host protein Past1, although might not directly interact with it, and that WalE1 manipulates host endocytosis. Yeast expressing WalE1 show deficiency in uptake of FM4-64 dye, and flies harboring mutations in Past1 or overexpressing WalE1 are sensitive to AgNO3, a hallmark of endocytosis defects. We also show that flies expressing WalE1 suffer from endocytosis defects in larval nephrocytes. Finally, we also show that Past1 null flies harbor more Wolbachia overall and in late egg chambers. Our results identify interactions between Wolbachia and a host protein involved in endocytosis and point to yet another important host cell process impinged upon by Wolbachia's WalE1 effector. |
| first_indexed | 2024-04-24T10:56:18Z |
| format | Article |
| id | doaj.art-59db4ef25688457a9038de3d91be37df |
| institution | Directory Open Access Journal |
| issn | 1553-7366 1553-7374 |
| language | English |
| last_indexed | 2024-04-24T10:56:18Z |
| publishDate | 2024-03-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS Pathogens |
| spelling | doaj.art-59db4ef25688457a9038de3d91be37df2024-04-12T05:31:06ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742024-03-01203e101124510.1371/journal.ppat.1011245The Wolbachia WalE1 effector alters Drosophila endocytosis.MaryAnn MartinSergio López-MadrigalIrene L G NewtonThe most common intracellular bacterial infection is Wolbachia pipientis, a microbe that manipulates host reproduction and is used in control of insect vectors. Phenotypes induced by Wolbachia have been studied for decades and range from sperm-egg incompatibility to male killing. How Wolbachia alters host biology is less well understood. Previously, we characterized the first Wolbachia effector-WalE1, which encodes an alpha-synuclein domain at the N terminus. Purified WalE1 sediments with and bundles actin and when heterologously expressed in flies, increases Wolbachia titer in the developing oocyte. In this work, we first identify the native expression of WalE1 by Wolbachia infecting both fly cells and whole animals. WalE1 appears as aggregates in the host cell cytosol. We next show that WalE1 co-immunoprecipitates with the host protein Past1, although might not directly interact with it, and that WalE1 manipulates host endocytosis. Yeast expressing WalE1 show deficiency in uptake of FM4-64 dye, and flies harboring mutations in Past1 or overexpressing WalE1 are sensitive to AgNO3, a hallmark of endocytosis defects. We also show that flies expressing WalE1 suffer from endocytosis defects in larval nephrocytes. Finally, we also show that Past1 null flies harbor more Wolbachia overall and in late egg chambers. Our results identify interactions between Wolbachia and a host protein involved in endocytosis and point to yet another important host cell process impinged upon by Wolbachia's WalE1 effector.https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1011245&type=printable |
| spellingShingle | MaryAnn Martin Sergio López-Madrigal Irene L G Newton The Wolbachia WalE1 effector alters Drosophila endocytosis. PLoS Pathogens |
| title | The Wolbachia WalE1 effector alters Drosophila endocytosis. |
| title_full | The Wolbachia WalE1 effector alters Drosophila endocytosis. |
| title_fullStr | The Wolbachia WalE1 effector alters Drosophila endocytosis. |
| title_full_unstemmed | The Wolbachia WalE1 effector alters Drosophila endocytosis. |
| title_short | The Wolbachia WalE1 effector alters Drosophila endocytosis. |
| title_sort | wolbachia wale1 effector alters drosophila endocytosis |
| url | https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1011245&type=printable |
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