The FRAC CAA Working Group was set up in 2005 to generate common resistance management recommendations for the Oomycete fungicides dimethomorph, flumorph, iprovalicarb, benthiavalicarb, mandipropamid and valifenalate.
All of the above-mentioned fungicides exhibit cross resistance and are grouped under the FRAC Code No. 40 in the FRAC Code List.
As shown in the table, the group name Carboxylic Acid Amides (CAA) has been chosen. This name best represents compounds from the three different chemical groups.
The mode of action of CAA compounds is directly linked to the inhibition of cellulose synthesis in the Oomycete plant pathogen (Blum et al. 2010).
Uptake studies with 14C labelled Mandipropamid (MPD) showed that this Oomycete control agent acts on the cell wall and does not enter the cell. Furthermore, 14C glucose incorporation into cellulose was perturbed in the presence of MPD. Gene sequence analysis of cellulose synthase genes in laboratory mutants, insensitive to MPD, revealed two point mutations in the PiCesA3 gene. This gene is known to be involved in cellulose synthesis. Both mutations in the PiCesA3 gene result in a change to the same amino acid (Glycine-1105) in the protein.
Sensitivity monitoring studies over several years revealed that in populations of the late blight pathogen, Phytophthora infestans, all isolates were fully sensitive to CAA fungicides. However, in populations of the grape downy mildew pathogen, Plasmopara viticola, isolates can be found in certain regions, which are resistant to all CAA fungicides.
Inheritance studies (Gisi et al. 2007) showed that sexual crosses between sensitive and CAA resistant isolates of Plasmopara viticola lead to a co-segregation of resistance to dimethomorph, iprovalicarb, benthiavalicarb and mandipropamid, but not to the phenylamide, mefenoxam, which was tested in parallel as an independent marker.
Further, the inheritance studies showed that the gene(s) for resistance to CAA fungicides are inherited in a recessive manner. Therefore, the entire F1 generation of crosses between sensitive and CAA resistant isolates was sensitive, and only in the F2 progeny did CAA resistance reappear in some isolates. These results suggest that the resistance risk can be classified as moderate (as compared to high for phenylamide and QoI fungicides) and that it can be managed by appropriate product use strategies.
Blum M, Waldner M, Gisi U. A single point mutation in the novel< i> PvCesA3</i> gene confers resistance to the carboxylic acid amide fungicide mandipropamid in Plasmopara viticola. Fungal Genetics and Biology 2010; 47(6): 499-510.
Gisi U, Waldner M, Kraus N, Dubuis PH, Sierotzki H. Inheritance of resistance to carboxylic acid amide (CAA) fungicides in Plasmopara viticola. Plant Pathology 2007; 56(2): 199-208.