To protect themselves from infection by disease-causing microbes, plants have systems that detect potentially harmful microbes and activate defence responses. Disease-causing microbes can overcome these defences by producing proteins called effectors that can enter host plant cells and disrupt them. Understanding what these effectors do in host plants could be useful for the development of more disease-resistant crop plants. Unfortunately, the roles of many effector proteins are not yet understood.
One of the ways effector proteins can interfere with plant defence responses is to prevent the relay of danger messages from the site of microbe detection at the plasma membrane to other locations in the cell. For the signal relays to function, the various protein components need to be located in the right places in the cell (plasma membrane, cytoplasm, nucleus, vacuole etc.). The cytoskeleton, consisting of filaments of the protein actin, is required for this organisation and moves proteins contained within (or on) small membrane-bound structures called vesicles.
In a paper recently published in PLOS Pathogens, the researchers studied an effector called HopW1, which increases the ability of Pseudomonas syringae to infect the model plant Arabidopsis thaliana (1). P. syringae also causes leaf diseases on crop species including wheat, tomato and peas. Infection can cause significant crop losses, for example wheat yields can decrease by over 50% (2).
The researchers found that HopW1 binds to and disrupts actin filaments in A. thaliana cells during infection. A pink fluorescent version of HopW1 was expressed in A. thaliana cells that had been treated to remove their cell wall. In these cells, a green fluorescent actin marker was also expressed. The figure below shows microscopy images of representative cells. The control cells that did not express HopW1 had a cross-crossing pattern of actin-filaments. However, in the HopW1-expressing cells very little actin was visible and it was only found around the edge in the same areas as the chloroplasts (shown in blue).
HopW1 also inhibited the targeting of proteins to internal cell compartments and disrupted the process by which vesicles are made from sections of plasma membrane and transported to other parts of the cell (endocytosis). By disrupting these processes, HopW1 is likely to be disrupting the signal relays between the site of bacterial recognition at the plasma membrane and other parts of the cell where defence responses are activated. Therefore, Hop1W can be thought of as a saboteur, crossing enemy lines and destroying communication lines to prevent the enemy from being able to mount an effective defence.
1) Kang, Y. et al (2014) HopW1 from Pseudomonas syringae disrupts the actin cytoskeleton to promote virulence in Arabidopsis. PLOS Pathogens.
2) Valencia-Botín, A.J. and Cisneros-López, M.E. (2007) A Review of the Studies and Interactions of Pseudomonas syringae Pathovars on Wheat. International Journal of Agronomy. http://www.hindawi.com/journals/ija/2012/692350/