A team of scientists at The Sainsbury Laboratory, led by Professor Silke Robatzek and in collaboration with Dr Matthieu Joosten from Wageningen University, have uncovered one of the mechanisms by which tomato plants can defend against disease-causing pathogens.
The perception of pathogens by plants, and how they relay these signals, is crucial to the outcome of immune responses. Increased understanding of the communication between plants and microbes could lead to new avenues for crop improvement.
Plants are under constant risk of infection by pathogens, such as bacteria and fungi. If these pathogens invade the plant they can cause serious and damaging infections. In order to prevent infections, plants have an innate immune system, which can detect pathogens and initiate defensive measures.
Professor Robatzek said,
“Receptors at the cell surface allow the plant to detect a pathogen attack. In order to activate the plant’s immune system these receptors need to transfer their information into the cell.”
Plant immunity relies on the early detection of pathogens by receptors located on the cell surface of plant cells. These receptors can detect microbial-derived, conserved molecular patterns or effector proteins that pathogens release upon entering the plant. Once the immune receptors have detected these microbe-derived effector proteins they send signals into the cell to initiate plant defensive measures.
In 1994, Professor Jonathan Jones and his group identified a tomato gene, Cf-9, that encodes a receptor-like protein which confers resistance to a specific strain of the tomato leaf mould fungus (Cladosporium fulvum). Receptor-like proteins, together with receptor kinases, are the two main types of plant immune receptors found on the surface of plant cells. Unlike receptor kinases, the receptor-like proteins have no signalling domain within the cell. It has therefore been a long-standing question how receptor-like proteins can activate intracellular signalling cascades.
The TSL team used live-cell imaging, gene silencing and coimmunoprecipitation to provide direct evidence of an interaction between Cf-4, a receptor-like protein, and BAK1/SERK3, a co-receptor kinase, thus finally answering this long-standing question by revealing the mechanism that initiates the Cf-4-induced immune response in tomato.
Read the paper here.
Dr Joosten said,
“Our research now shows that Cf-4 receptor-like proteins form a complex with the receptor kinase, BAK1/SERK3, which is known to form signalling complexes with immune receptor kinases in anti-bacterial immunity. Thus, there are fundamental biochemical similarities between receptor complexes of effector-sensing Cf receptors and receptor kinases sensing conserved bacterial molecular patterns.”
Professor Robatzek said,
“In addition we found that the Cf-4 receptor-like protein shows a dynamic subcellular localization pattern that depends on its activation status. This is reminiscent of how the anti-bacterial immune receptor kinases function in plants, revealing a conserved mode of action between receptor-like proteins and receptor kinases.”
22 years after the discovery of the tomato Cf-9 resistance gene, this new finding finally provides a mechanism by which receptor-like proteins can relay signals into the cell to trigger immune responses.
Professor Jonathan Jones said,
“When we discovered Cf proteins 22 years ago, they were the first immune receptors in plants or animals shown to carry extracellular leucine-rich repeats, and until now they have been viewed as somewhat anomalous. I am delighted to see this new mechanistic insight into how they work.”