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Querina (R) florina, apple variety resistant to apple scab. © INRA, LE LEZEC Marcel

Novel mechanisms for more sustainable resistance to disease

One avirulence precludes another (rapeseed)

Science has brought to light a negative interaction mechanism between two avirulence genes in phoma stem canker. In theory, this phenomenon renders the simultaneous presence of two corresponding resistance genes in the host plant futile.  However, if one of the two avirulence genes loses its avirulence - the corresponding rapeseed resistance gene no longer recognizing it – the other gene can then express its avirulence and the plant becomes resistant once again.

By Pascale Mollier, translated by Inge Laino
Updated on 03/31/2015
Published on 01/22/2015

Necrosis of rapeseed crown caused by phoma stem canker. © Marie-Hélène Balesdent and Thierry Rouxel, Marie-Hélène Balesdent et Thierry Rouxel
Necrosis of rapeseed crown caused by phoma stem canker © Marie-Hélène Balesdent and Thierry Rouxel, Marie-Hélène Balesdent et Thierry Rouxel

Combining several genes that are resistant to a given pathogen in a host plant is a common strategy for boosting the sustainability of resistance and delaying circumvention. It is indeed quite logical to expect that a pathogen will have a tougher time circumventing several, as opposed to one, sources of resistance.

However, there are cases where it is not as simple as that…

Researchers from five INRA teams have proven so with phoma stem canker in rapeseed (Leptosphaeria maculans). In this case, the combination of two resistance genes is futile, since only one expresses itself at a time. However, when one of the resistance genes is circumvented, the other can express itself efficiently to maintain resistance to phoma stem canker. In this atypical case, the question is: what is the best strategy for managing resistance and boosting sustainability?

Resistance and avirulence

A molecular dialogue takes place between a pathogen and its host plant that is often likened to an “arms race”. The pathogen has virulence determinants, called “effectors”, that the plant learns to recognise, and against which it develops targeted resistance thanks to an adaptive evolutionary mechanism. When an effector is thus “unmasked”, it triggers resistance against the pathogen in the plant. The gene that encodes this effector in the pathogen then becomes an avirulence gene, since the expression of the effector reduces the virulence of the pathogen.

In the case of phoma stem canker in rapeseed, several avirulence genes have been identified and cloned. Two of them were the subject of particularly close study, since they represent a rare case of negative interaction. That is, the expression of one hinders the effect of the other.

Negative interaction in avirulence genes

The avirulence genes AvrLm7 and AvrLm3 are present in natural populations of rapeseed phoma stem canker in France. These phoma genes correspond to two resistance genes in rapeseed called Rlm7 and Rlm3, respectively. When one of these two resistance genes is present in rapeseed, it recognises the effector encoded by the corresponding avirulence gene, triggering a resistance response in the plant against the pathogen.

However, scientists have observed that the expression of one avirulence gene inhibits the avirulence effect of the other. In other words, when Rlm7 is present in rapeseed, the resistance response is triggered against the effector encoded by AvrLm7, but at the same time, Rlm3 resistance is deactivated. That is, the effector encoded by AvrLm3 is no longer recognised by the Rlm3 product. The mechanism of this interaction is still unknown, but thought to be protein-based, whether between the two effectors or between effector and resistance proteins. Indeed, research has shown that the inhibition does not stem from avirulence gene expression.

This mechanism is logical from the “point of view” of the pathogen, since it leads to a weaking of avirulence.

“From the point of view of protecting plants, this antagonism between avirulence genes opens doors for managing resistance to phoma stem canker. Monogenetic Rlm7 resistance was progressively rolled out starting in 2004 in a number of rapeseed varieties in France, and reports of circumvention begin to appear in 2010-2011, with the emergence of virulent phoma strains vis-à-vis Rlm7. However, strains that circumvent Rlm7, that is, strains that are no longer Rlm7-avirulent, are avirulent for Rlm3, since the antagonism disappears. Resistance to Rlm3 can therefore be exploited to counter-select virulent strains vis-à-vis Rlm7, and therefore to boost the sustainability of Rlm7, while it was of no interest when Rlm7 was still effective”, concludes Marie-Hélène Balesdent, head of the K Masstec programme (1).

Researchers are now looking for the best way to combine resistance genes, simultaneously or progressively, by measuring and modelling the effect of different strategies on the frequency of virulent strains in pathogen populations. They are also striving to understand the molecular basis for this atypical interaction, thanks to the recent cloning of the AvrLm3 gene.

(1) K Masstec programme: Knowledge-driven design of management strategies for stem canker specific resistance genes.

Scientific contact(s):

Associated Division(s):
Plant Health and Environment
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Rapeseed phoma stem canker

On a global scale, phoma stem canker (or necrosis of rapeseed crown) is one of the most devastating diseases of rapeseed, known to cut yields by up to 50%. While combatting the pathogen by chemical means is not very effective, the use of rapeseed varieties that are naturally resistant to Leptosphaeria maculans, the fungus that causes the infection, is widespread.