Heteroplasmy of the cytochrome b Gene in Venturia inaequalis and Its Involvement in Quantitative and Practical Resistance to Trifloxystrobin

Abstract

Quantitative (partial) and qualitative (complete) resistance responses to quinone outside inhibitor (QoI) fungicides have been documented for the apple scab pathogen Venturia inaequalis. Resistance monitoring efforts have traditionally focused on the detection of qualitative resistance based on a single point mutation, G143A, within the cytochrome b (cyt b) gene. In order to better understand the role of heteroplasmy of the cyt b gene in the QoI resistance response for isolates and populations of V. inaequalis, an allele-specific quantitative polymerase chain reaction was developed to quantify the relative abundance of the A143 (resistant) allele in 45 isolates of V. inaequalis with differing in vitro resistance responses to the QoI fungicide trifloxystrobin. Although a high relative abundance of the A143 allele (>62%) was associated with isolates with high resistance responses (50 to 100% relative growth on trifloxystrobin-amended medium), heteroplasmy of the cyt b gene was not the primary factor involved in isolates with moderate resistance responses (29 to 49% relative growth). The relative abundance of the A143 allele in isolates with moderate resistance to trifloxystrobin rarely exceeded 8%, suggesting that other resistance mechanisms are involved in moderate resistance and, therefore, that the Qol resistance response is polygenic. In research orchards where QoI fungicides failed to control apple scab (practical resistance), field trials were conducted to demonstrate the link between practical resistance and the abundance of the A143 allele. Relative abundance of the A143 allele in these orchard populations exceeded 20% in 2011 and 2012. Similarly, of the eight additional commercial orchards screened in 2011, the relative abundance of the A143 allele always exceeded 20% in those with QoI practical resistance. Although heteroplasmy of the cyt b gene did not entirely explain the response of isolates with moderate resistance to QoIs, the relative abundance of A143 in orchard populations of V. inaequalis helps to explain the point of emergence for practical resistance to trifloxystrobin across several orchard populations with differing production histories.

Investigation of the sensitivity of Plasmopara viticola to amisulbrom and ametoctradin in French vineyards using bioassays and molecular tools

“…Podosphaera leucotricha ). It has even been described for the G143A mutant allele associated with QoI resistance in Venturia inaequalis , Podosphaera xanthii and Botrytis cinerea . Further investigations are necessary to determine if mixed alleles in one lesion are caused by mixed strains in the same lesion or by mixed mitochondrial DNA in same strain, but monosporangial isolation in resistant populations seemed to confirm that multiple‐allele detection was at least partly due to heteroplasmy in P. viticola strains.…”

Cloning of the Cytochrome b Gene From the Tomato Powdery Mildew Fungus Leveillula taurica Reveals High Levels of Allelic Variation and Heteroplasmy for the G143A Mutation

“…To moderate the fitness cost associated with the G143A mutation, many fungi are shown to exhibit mitochondrial heteroplasmy for the cytb gene and particularly for the G143A substitution (Lesemann et al, 2006; Villani and Cox, 2014; Vielba-Fernandez et al, 2018). Heteroplasmy is commonly described as the coexistence of more than one type of mitochondrial genomes (mitotypes) in a single cell and although it regularly occurs in plants, it is less often described in fungi (Barr et al, 2005; Woloszynska, 2009; Wilson and Xu, 2012).…”

Long term field sampling in Sweden reveals a shift in occurrence of cytochrome b genotype and amino acid substitution F129L in Alternaria solani, together with a high incidence of the G143A substitution in Alternaria alternata

“…Further, the mitochondria may be inherited in different ratios and result in isolates that vary in tolerance against strobilurins. (Lesemann et al 2006;Villani and Cox 2014). During this study, there were a few samples that had peaks of both nucleotides, but they were considered as mutated since the peak of the A-nucleotide was in general higher than the C-nucleotide peak.…”