Arthropod autophagy molecules facilitate Anaplasma phagocytophilum infection of Ixodes scapularis tick cells
Abstract Ixodes scapularis ticks transmit several medically important pathogens including Anaplasma phagocytophilum to humans and animals. In this study, we provide evidence that A. phagocytophilum modulates autophagy molecules for its survival in tick cells. qRT-PCR analysis revealed that A. phagoc...
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Nature Portfolio
2025-03-01
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| Series: | Communications Biology |
| Online Access: | https://doi.org/10.1038/s42003-025-07859-6 |
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| author | Jeremy W. Turck Hameeda Sultana Girish Neelakanta |
| author_facet | Jeremy W. Turck Hameeda Sultana Girish Neelakanta |
| author_sort | Jeremy W. Turck |
| collection | DOAJ |
| description | Abstract Ixodes scapularis ticks transmit several medically important pathogens including Anaplasma phagocytophilum to humans and animals. In this study, we provide evidence that A. phagocytophilum modulates autophagy molecules for its survival in tick cells. qRT-PCR analysis revealed that A. phagocytophilum infection results in the upregulation of tyrosine phosphatase, shp-2, and serine/threonine-protein kinase, mTOR, in ticks and tick cells. RNAi-mediated knockdown of shp-2 or functional blocking with SHP-2 inhibitor resulted in significantly increased bacterial burden and reduced phospho-mTOR levels in A. phagocytophilum-infected tick cells. In addition, treatment of A. phagocytophilum-infected tick cells with rapamycin (mTOR inhibitor) resulted in significantly increased bacterial burden and reduced phospho-mTOR levels. Furthermore, expression of autophagy molecules such as atg14 and ulk1 were noted to be upregulated in both A. phagocytophilum-infected unfed ticks and tick cells. RNAi-mediated silencing of atg14 or ulk1 affected bacterial growth in tick cells. Collectively, these results not only indicate distinct host and pathogen responses in tick-A. phagocytophilum interactions but also suggest that this bacterium modulates autophagy molecules for its survival in ticks. |
| format | Article |
| id | doaj-art-2dd35fda1334493389e70a6700db2dbd |
| institution | DOAJ |
| issn | 2399-3642 |
| language | English |
| publishDate | 2025-03-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Communications Biology |
| spelling | doaj-art-2dd35fda1334493389e70a6700db2dbd2025-08-20T02:56:20ZengNature PortfolioCommunications Biology2399-36422025-03-018111110.1038/s42003-025-07859-6Arthropod autophagy molecules facilitate Anaplasma phagocytophilum infection of Ixodes scapularis tick cellsJeremy W. Turck0Hameeda Sultana1Girish Neelakanta2Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of TennesseeDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of TennesseeDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of TennesseeAbstract Ixodes scapularis ticks transmit several medically important pathogens including Anaplasma phagocytophilum to humans and animals. In this study, we provide evidence that A. phagocytophilum modulates autophagy molecules for its survival in tick cells. qRT-PCR analysis revealed that A. phagocytophilum infection results in the upregulation of tyrosine phosphatase, shp-2, and serine/threonine-protein kinase, mTOR, in ticks and tick cells. RNAi-mediated knockdown of shp-2 or functional blocking with SHP-2 inhibitor resulted in significantly increased bacterial burden and reduced phospho-mTOR levels in A. phagocytophilum-infected tick cells. In addition, treatment of A. phagocytophilum-infected tick cells with rapamycin (mTOR inhibitor) resulted in significantly increased bacterial burden and reduced phospho-mTOR levels. Furthermore, expression of autophagy molecules such as atg14 and ulk1 were noted to be upregulated in both A. phagocytophilum-infected unfed ticks and tick cells. RNAi-mediated silencing of atg14 or ulk1 affected bacterial growth in tick cells. Collectively, these results not only indicate distinct host and pathogen responses in tick-A. phagocytophilum interactions but also suggest that this bacterium modulates autophagy molecules for its survival in ticks.https://doi.org/10.1038/s42003-025-07859-6 |
| spellingShingle | Jeremy W. Turck Hameeda Sultana Girish Neelakanta Arthropod autophagy molecules facilitate Anaplasma phagocytophilum infection of Ixodes scapularis tick cells Communications Biology |
| title | Arthropod autophagy molecules facilitate Anaplasma phagocytophilum infection of Ixodes scapularis tick cells |
| title_full | Arthropod autophagy molecules facilitate Anaplasma phagocytophilum infection of Ixodes scapularis tick cells |
| title_fullStr | Arthropod autophagy molecules facilitate Anaplasma phagocytophilum infection of Ixodes scapularis tick cells |
| title_full_unstemmed | Arthropod autophagy molecules facilitate Anaplasma phagocytophilum infection of Ixodes scapularis tick cells |
| title_short | Arthropod autophagy molecules facilitate Anaplasma phagocytophilum infection of Ixodes scapularis tick cells |
| title_sort | arthropod autophagy molecules facilitate anaplasma phagocytophilum infection of ixodes scapularis tick cells |
| url | https://doi.org/10.1038/s42003-025-07859-6 |
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