Maize is one of the most important crops in the world. It is a major nutritional ingredient in Africa and South America and it is also widely used as an animal feed and to produce biofuels. Hundreds of years of domestication and breeding allowed the evolution from the wild grass teosinte originated in Mexico to the highly productive maize cobs we now know. Despite this extensive breeding, many maize plants are still susceptible to some plant diseases caused by plant pathogens.
To fight these pests, current research tries to understand how we can make our plants more resistant to such pathogens. The last years of research have shown that the soil in which the plants are growing can make a dramatic difference. Soil houses a diverse community of microorganisms including bacteria and fungi (for more information you can also have a look into Jia Yu’s and Paloma Durán’s Planter’s Punches). Many of these microorganisms were shown to be antagonists of pathogens. For example, these antagonists can compete against the pathogens and fight them actively. Therefore, these antagonists are of high interest for breeders and for the fight against pests.
To understand how these “healthy” soils work, we try to understand how plants specifically select for these “good” microbes, while at the same time the plant restricts pathogens. It is quite surprising, that the plant can distinguish those microbes, since “good” and “bad” microbes “look” similar to the plant. In addition, plant’s defense mechanisms will likely not distinguish between these “good and bad guys”. Past research has already shown that plants enrich the area close to their roots, called rhizosphere, with microbes beneficial to themselves.
We now try to understand how the “good” bacteria can tell the plant that they are actually “good guys”. Our hypothesis is, that these bacteria can outsmart plant recognition. To identify pathogens, the plant releases so-called “proteases” into the space outside of the plant cell, which is called the “apoplast”. These apoplastic proteases function as sensors cleaving proteins, as for example proteins of the bacterial outer layer present in the apoplast. When these bacterial proteins are cut into small pieces, also called peptides, these pieces can be recognized by the plant. The recognition of these pieces triggers the plant defense response and the fight against the intruder starts.
We think that these “good” bacteria might be able to prevent the cleavage of their own proteins with a so-called inhibitor. These inhibitor molecules inactivate the proteases and impair their function. Thereby, they cannot release peptides anymore and the recognition of the microbe by the plant is stopped. This mechanism of inhibition has also been well described for different pathogens infecting different plant species.
To prove our hypothesis, we tried to find bacterial protease inhibitors in a commensal community (the “good guys”) found in the roots of maize. Thereby I have found one inhibitor candidate confirming our hypothesis! Now we want to know whether the bacterium really needs this inhibitor to prevent the recognition by the plant. We also want to know whether the bacterium with this inhibitor has an advantage over other bacteria or whether it can help other bacteria in a symbiotic way. For example, this inhibitor could allow other microbes to be also not detected by the plant proteases.
Understanding this interaction between plants and microbes might help us to develop natural strategies to protect our maize plants from future pests.
Under the heading Planter’s Punch we present each month one special aspect of the CEPLAS research programme. All contributions are prepared by our early career researchers.
Daniel Moser is a doctoral researcher in the group of Prof. Doehlemann in the Institute for Terrestrial Microbiology at the University of Cologne. His research focuses on the understanding of the modulation of plant papain-like cysteine proteases in complex microbial interactions. Before joing CEPLAS, he studied Biochemistry at the Heinrich-Heine University Düsseldorf and performed research abroad at Michigan State University in USA.