panel de control Archives - Gen9 Genetics
Sensitivity to fungicides is strongly favored by selection and increases rapidly in frequency in selected populations (McDonald and Linde 2002; van den Bosch and Gilligan2008; van den Bosch et al. 2011). The genetic architecture associated with resistant phenotypes will arise from a complex set of mutations and their interactions, which in turn will be affected by the biology of the pathogen population and the characteristics of the fungicide. The mode of action (such as impaired mitochondrial respiration, Yang et al. 2011) and the number of target sites (single-site versus multiple-site fungi) will play a key role in defining resistance pathways. and McDonald 2015), innate resistance and epistatic effects will also significantly shape the evolutionary process of resistance emergence (Lucas et al. 2015). Therefore, deciphering the genetic architecture of emerging fungicide resistance can provide useful information and potentially identify the key factors that govern evolutionary responses of pathogens. Fungicides of the demethylation inhibitor (DMI) family are the molecules most used in agriculture and human medicine (Fisher et al. 2018). The mode of action is to hinder ergosterol biosynthesis by inhibiting the enzyme 14a-demethylase (CYP51), which negatively affects the integrity and permeability of the fungal cell membrane (Georgopapadakou and Walsh 1996;
Lass-Flo¨ rl 2011). In this group of fungicides, resistance arises through different mechanisms, including 1) amino acid mutations in the target protein, 2) overexpression of the gene encoding the target protein, and 3) enhanced transporter activity that reduces intracellular concentrations of the fungicide. (Becher and Wirsel2012; Cools and Fraaije 2013). Importantly, resistance in populations can be based on multiple mechanisms and is likely to be limited by the costs of fitness (Zhan and McDonald 2013; Mikaberidze and McDonald 2015). Resistance can also arise multiple times independently within species (Torriani et al. 2009). Structural changes in the CYP51 protein are considered the most common mechanism leading to interspecies resistance (Deng et al. 2007; Lucas et al. 2015). Highly resistant genotypes can acquire dozens of different mutations in the CYP51 gene in a staggered fashion (Coolsand Fraaije 2013). The consequences of the staggered accumulation of mutations are complex interactions with the genetic background and the selection of compensatory mutations (Cools et al. 2010; Lucas et al. 2015; Mullis et al. 2018). Alternative mechanisms for point mutations include variation in the copy number of CYP51 paralogs that are common in Ascomycota fungi (Deng et al. 2007; Liu et al. 2011; Yanet al. 2011; Brunner et al. 2016). The lack of knowledge about resistance mutations that occur outside the CYP51 gene limits our understanding of the possible importance of interactions between resistance mutations that occur in other genes. acquired within the species