Popular Science: Armed plant pathogens
Plant defence mechanisms consist of several layers. Upon the very first contact with a pathogen, the plant can perceive conserved molecular structures that can be typically found either on the pathogen’s surface or inside its cells. Subsequently the plant’s defence mechanisms are activated using phytohormone signalling pathways. These mechanisms include cell wall thickening, which makes it harder for the pathogens to enter the host plant cells, or the production of toxins and reactive oxygen species, which can directly kill the pathogen or stop its growth in the plant tissue. The protein of bacterial flagella flagelin and bacterial protein Et-Tu which is required for DNA replication are known examples of the aforementioned perceived structures.
Pathogens were forced to overcome plant defences and so they evolved a certain weapon called effectors. The effectors are small proteins secreted into intercellular space or directly into the host cell cytoplasm. In the host the effectors interfere with the plant’s defence. Plants then evolved a second layer of defence by creating specific receptors which perceive the effectors.
Scientists from the Laboratory of Pathological Plant Physiology at IEB AS CR in collaboration with the Department of Biochemistry of The Faculty of Science are interested in the characterization of specific effectors of the pathogenic fungus Leptosphaeria maculans. The fungus is a causal agent of the blackleg disease in oilseed rape plants and it is considered to be the most important pathogen of the oilseed rape in Europe and Australia. The last characterized effector until now was named AvrLm4-7.
Using two genetically very similar isolates of L. maculans that differ in the ability to produce the effector AvrLm4-7, the scientists found that this protein significantly contributes to the aggressiveness of the pathogen. Experimental plants were divided into two groups. One was infected with an L. maculans isolate producing AvrLm4-7 and the other was infected with an isolate that is not able to produce the effector. Symptoms of the disease were quantified and compared between the two groups after 13 days. The necrotic area of infected leaves was about 40% higher in plants that were infected with the fungus producing AvrLm4-7.
To determine the cause of increased leaf necrosis the plants’ triggered defence mechanisms were subsequently analysed. The suppression of activity of specific phytohormone signalling pathways was observed in plants infected with the fungus producing AvrLm4-7. The suppressed pathways are mediated by salicylic acid and ethylene and are involved in danger perception and the activation of defence mechanisms. One such mechanism is an increase in the production of reactive oxygen species in the infected tissue which was significantly lower in plants infected with the more aggressive isolate.
Leptosphaeria maculans uses the AvrLm4-7 protein to confuse plant defence signalling which lowers the plant’s ability to respond to the pathogen attack. If the observed decrease in the reactive oxygen species production is a direct consequence of plant signalling deactivation or the effector is involved in some other processes remains to be elucidated. Hopefully, the study will help us better understand the interplay between plants and their pathogens and prevent for example crop failures in the future.
Hana Krutinová
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