by Farhan and Daniel
The evolution of azole resistance in agricultural fields
Our paper on multilocus resistance evolution to azoles in a fungal plant pathogen is online now.
The evolution of fungicide resistance is truly worrisome for farmers and at the same time extremely fascinating as a case study of rapid adaptive evolution.
One of the most commonly used classes of fungicides are azoles. Resistance to azoles has been well established in human and animal pathogenic fungi, and includes a wide array of mechanisms to cope with stress induced by fungicides. The analysis of resistance in plants pathogens was largely focused on mutations in a specific gene called CYP51. This gene encodes the protein that is directly targeted by azoles. Additional mechanisms were rarely explored in field populations.
We studied an ubiquitous pathogen of barley called Rhynchosporium commune. We obtained a pathogen collection across the world comprising regions where fungicides were used frequently and others were the pathogen was unlikely to have been exposed yet. Then, we sequenced the entire genome of all strains and screened for loci associated with increased resistance to azoles. For this, we used genome-wide association mapping (or GWAS), which is a widely used tool in human and plant genetics.
Our study that just came out in Molecular Ecology showed that several previously unknown genes contributed to azole resistance. These genes encoded for proteins related to stress responses, regulation of transcription and other processes. Then, we analyzed whether some mutations that conferred higher resistance had an impact on the growth of the fungus. We found that some mutations had no detectable impact on growth and are likely to become fixed in resistant populations. But we also found resistance mutations that were associated with slower growth. Such trade-offs in the evolution of resistance (or "cost of resistance") are important, because we may be able to exploit such "weaknesses" of the pathogen to devise more sustainable control strategies.
The evolution of azole resistance in agricultural fields
Our paper on multilocus resistance evolution to azoles in a fungal plant pathogen is online now.
The evolution of fungicide resistance is truly worrisome for farmers and at the same time extremely fascinating as a case study of rapid adaptive evolution.
One of the most commonly used classes of fungicides are azoles. Resistance to azoles has been well established in human and animal pathogenic fungi, and includes a wide array of mechanisms to cope with stress induced by fungicides. The analysis of resistance in plants pathogens was largely focused on mutations in a specific gene called CYP51. This gene encodes the protein that is directly targeted by azoles. Additional mechanisms were rarely explored in field populations.
We studied an ubiquitous pathogen of barley called Rhynchosporium commune. We obtained a pathogen collection across the world comprising regions where fungicides were used frequently and others were the pathogen was unlikely to have been exposed yet. Then, we sequenced the entire genome of all strains and screened for loci associated with increased resistance to azoles. For this, we used genome-wide association mapping (or GWAS), which is a widely used tool in human and plant genetics.
Our study that just came out in Molecular Ecology showed that several previously unknown genes contributed to azole resistance. These genes encoded for proteins related to stress responses, regulation of transcription and other processes. Then, we analyzed whether some mutations that conferred higher resistance had an impact on the growth of the fungus. We found that some mutations had no detectable impact on growth and are likely to become fixed in resistant populations. But we also found resistance mutations that were associated with slower growth. Such trade-offs in the evolution of resistance (or "cost of resistance") are important, because we may be able to exploit such "weaknesses" of the pathogen to devise more sustainable control strategies.