Strauch Claudia Janina, Sprotte Nico, Peña Lozano Estefania, Boutant Emmanuel, Amari Khalid, Ostendorp Steffen, Ostendorp Anna, Kehr Julia, Niehl Annette
Institute for Epidemiology and Pathogen Diagnostics, Julius Kühn Institute (JKI) - Federal Research Centre for Cultivated Plants, Messeweg 11-12, 38104, Brunswick, Germany.
Institute of Plant Science and Microbiology, University of Hamburg, Ohnhorststr. 18, Hamburg, 22609, Germany.
Virol J. 2025 May 7;22(1):134. doi: 10.1186/s12985-025-02757-z.
Plant viral movement protein (MP) function is decisive for virus cell-to-cell movement. Often, MPs also induce membrane alterations, which are believed to play a role for the establishment of viral replication compartments. Despite these central roles in virus infection, knowledge of the underlying molecular mechanisms by which MPs cause changes in plasmodesmata (PD) size exclusion limit and contribute to the formation of viral replication compartments remain far from being complete.
To further identify host processes subverted by viral MPs, we here characterized the MP of Japanese soil-borne wheat mosaic virus (JSBWMV). We used confocal fluorescence microscopy to study the subcellular localization of MP and to address its functionality in promoting virus cell-to-cell movement. Using the biochemical and biophysical methods co-immunoprecipitation, fluorescence lifetime imaging, microscale thermophoresis and RNA immunoprecipitation we investigate the capacity of MP to multimerize and to bind viral and cellular RNAs.
MP localized to PD, promoted cell-to-cell movement by complementing a movement-deficient unrelated virus, formed multimers in-vivo and bound to viral RNA with high affinity. Using RNA immunoprecipitation, we identified host RNAs associated with the viral MP. Within the MP-RNA complexes we found RNAs encoding proteins with key functions in membrane modification, signaling, protein folding, and degradation. We propose that binding of MP to these RNAs during infection and regulation of their spatio-temporal translation may represent a mechanism for MPs to achieve PD and host control during replication and movement.
This study provides new insight into the complex interactions between viral MPs and host cellular processes.
植物病毒运动蛋白(MP)的功能对于病毒在细胞间的移动起决定性作用。通常,MP还会诱导膜的改变,人们认为这在病毒复制区室的形成中发挥作用。尽管MP在病毒感染中起着这些核心作用,但对于MP导致胞间连丝(PD)大小排阻极限发生变化并促进病毒复制区室形成的潜在分子机制,我们的了解仍远未完整。
为了进一步确定被病毒MP颠覆的宿主过程,我们在此对日本土传小麦花叶病毒(JSBWMV)的MP进行了表征。我们使用共聚焦荧光显微镜研究MP的亚细胞定位,并探讨其在促进病毒细胞间移动方面的功能。我们使用免疫共沉淀、荧光寿命成像、微量热泳动和RNA免疫沉淀等生化和生物物理方法,研究MP多聚化以及结合病毒和细胞RNA的能力。
MP定位于PD,通过互补一种运动缺陷型无关病毒促进细胞间移动,在体内形成多聚体,并与病毒RNA高亲和力结合。通过RNA免疫沉淀,我们鉴定了与病毒MP相关的宿主RNA。在MP-RNA复合物中,我们发现了编码在膜修饰、信号传导、蛋白质折叠和降解中具有关键功能的蛋白质的RNA。我们提出,在感染过程中MP与这些RNA的结合及其时空翻译的调控可能代表了MP在复制和移动过程中实现对PD和宿主控制的一种机制。
本研究为病毒MP与宿主细胞过程之间的复杂相互作用提供了新的见解。