The Pseudomonas syringae Type III Effector HopG1 Induces Actin Remodeling to Promote Symptom Development and Susceptibility during Infection
| العنوان: | The Pseudomonas syringae Type III Effector HopG1 Induces Actin Remodeling to Promote Symptom Development and Susceptibility during Infection |
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| المؤلفون: | Jessica L. Henty-Ridilla, Brian H. Kvitko, Allison L. Creason, Jeff H. Chang, Christopher J. Staiger, Yi-Ju Lu, Katie Porter, Masaki Shimono, Sheng Yang He, Brad Day |
| المصدر: | Plant Physiology. 171:2239-2255 |
| بيانات النشر: | Oxford University Press (OUP), 2016. |
| سنة النشر: | 2016 |
| مصطلحات موضوعية: | 0106 biological sciences, 0301 basic medicine, Physiology, Effector, fungi, Actin filament organization, food and beverages, Actin remodeling, macromolecular substances, Plant Science, Biology, Actin cytoskeleton, 01 natural sciences, Cell biology, 03 medical and health sciences, 030104 developmental biology, Profilin, Genetics, biology.protein, Kinesin, Cytoskeleton, Actin, 010606 plant biology & botany |
| الوصف: | The plant cytoskeleton underpins the function of a multitude of cellular mechanisms, including those associated with developmental- and stress-associated signaling processes. In recent years, the actin cytoskeleton has been demonstrated to play a key role in plant immune signaling, including a recent demonstration that pathogens target actin filaments to block plant defense and immunity. Herein, we quantified spatial changes in host actin filament organization after infection with Pseudomonas syringae pv. tomato DC3000 (Pst DC3000), demonstrating that the type-III effector HopG1 is required for pathogen-induced changes to actin filament architecture and host disease symptom development during infection. Using a suite of pathogen effector deletion constructs, coupled with high-resolution microscopy, we found that deletion of hopG1 from Pst DC3000 resulted in a reduction in actin bundling and a concomitant increase in the density of filament arrays in Arabidopsis, both of which correlate with host disease symptom development. As a mechanism underpinning this activity, we further show that the HopG1 effector interacts with an Arabidopsis mitochondrial-localized kinesin motor protein. Kinesin mutant plants show reduced disease symptoms after pathogen infection, which can be complemented by actin-modifying agents. In total, our results support a model in which HopG1 induces changes in the organization of the actin cytoskeleton as part of its virulence function in promoting disease symptom development. |
| تدمد: | 1532-2548 0032-0889 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_________::46b92d4f0dea5b0d624ac737a4b056e5Test https://doi.org/10.1104/pp.16.01593Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi...........46b92d4f0dea5b0d624ac737a4b056e5 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15322548 00320889 |
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