Plants use mobile proteins to defend themselves against bacteria

Immune response depends on the distribution of plant and bacterial proteins

December 09, 2011

When a resistant plant detects a bacterial infection, it must react fast and appropriately. It will halt bacterial growth, sacrifice the cells in the infected area, and sound the alarm throughout the plant. The precise reaction depends on where the relevant bacterial protein is located: in the nucleus, in the cytoplasm, or in both. Jane Parker and her colleagues at the Max Planck Institute for Plant Breeding Research in Cologne have now discovered how the different immune responses are triggered.

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Resistant plants are not unprepared for intruders. Their cells are supplied with receptors that detect danger, as well as a mobile crisis manager responsible for the rollout of the immune response. As long as the plant is undisturbed, the receptors and crisis manager lie in wait in the cytoplasm and the cell nucleus, on the lookout for any unwelcome visitors.

Invading bacteria also come ready to tackle their opponents, bringing molecular equipment designed to help them put the plant’s immune system out of service. This tool is called an effector and gains entry to the cells through a molecular needle. It is not yet clear how the battle between the resistant plant and its adversaries begins, but it is probable that the bacterial effector takes on the crisis manager. The plant may become aware of the attack because its receptors are keeping watch over the protein.

Katharina Heidrich and Jane Parker, along with other colleagues, have now discovered what happens after an alarm is triggered and how the role of the crisis manager switches from a possible sensor to a coordinator for the ongoing immune response. Key factors would seem to be where the plant receptor, the bacterial effector and the crisis manager EDS1 travel in the cell after the alarm has sounded, and what agreements they reach in the process.

In order for bacterial proliferation to be suppressed, the bacterial effector must move from the cytoplasm into the nucleus, where it will come into contact with the receptor and the crisis manager. It will then no longer be required in the cytoplasm for this type of immune response. All three proteins must be active in both the nucleus and the cytoplasm in order to induce cell death in the infected cells and send the alarm throughout the plant. This seems to involve close communication between the two compartments.

Until now, the scientists knew very little about what happens after an intruder has been detected. “The plant has to distinguish between the different options with great care. Every immune reaction takes energy and is detrimental to growth. The plant cannot afford to react to a trifling attack with the full fury of its immune system. On the other hand, it must not make the mistake of downplaying a serious attack, or it will run the danger of being destroyed”, explains Jane Parker. The intracellular mobility of receptors, effectors and crisis managers leads the immune response in different directions. It is thought that EDS1 has a double role. It could be the protein tackled by the bacterial effector and it mediates the immune response, because, after the alarm is sounded, it must be present in both the nucleus and the cytoplasm.

The research was conducted using the model plants Arabidopsis and tobacco. For the purpose of their experiments, the scientists attached a signal to the active part of the bacterial effector which either gets the whole amount into the cell nucleus or keeps it out. This enabled the scientists to observe that the bacterial effector finds its way into both compartments. The containment of bacterial growth, however, is linked to the presence of both the effector and the receptor in the nucleus. If the effector is kept out of the cytoplasm, this immune reaction is uncoupled from the programmed death of infected cells. “This means that cell death per se does not stand for full resistance. It is only one possible pathway out of a crisis”, explains Katharina Heidrich.

Heidrich, Parker and their colleagues have yet to discover exactly what the three proteins do in the cell compartments in order to set off an immune response. However, they have shown that both the plant receptor and the bacterial effector form complexes with the crisis manager in the cell nucleus. Whether these complexes prepare the transcription of important resistance genes or are perhaps themselves involved in the transcription process, is as yet unknown. Also unclear is how the dialogue between the three proteins in the nucleus and the cytoplasm lead to programmed cell death or a generalised immune response. What this research does show however, is where to look for the answers.


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