Mutations of the β-Tubulin Gene Associated with Different Phenotypes of Benzimidazole Resistance in the Cereal Eyespot Fungi Tapesia yallundae and Tapesia acuformis

Following the dynamics of strobilurin resistance in Blumeria graminis f.sp. tritici using quantitative allele‐specific real‐time PCR measurements with the fluorescent dye SYBR Green I

“…(Albertini et al , 1999). Although mutations at 10 sites within the β -tubulin gene can confer benzimidazole resistance (Davidse & Ishii, 1995), only a few have been found in field populations of fungi, probably due to reduced fitness and /or pathogenicity linked with certain mutations.…”

Novel point mutations in β-tubulin gene for carbendazim resistance maintaining nematode pathogenicity of Paecilomyces lilacinus

“…The principle of benzimidazole resistance is closely associated with point mutations in the β-tubulin genes that change the structure of the fungicide-binding point (Gafur et al 1998;Albertini et al 1999;Peres et al 2004;Chung et al 2006;Davidson et al 2006;Ziogas et al 2009). T274I, R282Q, and Q292E mutations significantly weakened the interactions and binding of the drugs taxol and epothilone (Natarajan and Senapati 2012), while Q43P and R318W mutations had a significant impact on platelet physiology in immune thrombocytopenia (Freson et al 2005;Kunishima et al 2009;NavarroNunez et al 2011).…”

Detection of Fungicide Resistance

“…Sequence analysis of the -tubulin gene showed that a single base pair mutation at codon 6 was responsible for the low resistance level to benzimidazoles in all the LR isolates of M. fructicola examined. Curiously, different substitutions at the same codon resulted in different degrees of resistance in the cereal eyespot fungus, Tapesia yallundae (Pseudocercosporella herpotrichoides): codon changes from Glu to Ala, Gly, Lys, and Gln at position 198 had 50% effective concentration (EC50) values to carbendazim ranging from 0.5 to more than 25 m g/ml in some isolates (Albertini et al, 1999), one of the first instances that demonstrates that differences in genetic background may play a role in expression of specific fungicide resistance genes.…”

“…For example, most fungicides for the control of Chromista (e.g., mefenoxam, fluopicolide, dimethomorph) do not control true fungi; some fungicides are specific for ascomycete (e.g., thiophanate-methyl) or basidiomycete fungi (flutolanil), and species within the same genus of fungi may respond differently to certain fungicides (Leroux et al 2012). Additionally, different genotypes exist within a spectrum of sensitive to resistant (Albertini et al 1999). The relationship between the frequency of fungicide application and resistance has been established (King and Griffin, 1985;Suzuki et al 2010), and the role of rate or dose in this process is deserving of further study (Genet et al 2006;van den Bosche et al 2011).…”

“…Usually, resistant individuals are detected using bioassays (sensitivity tests or poison plate assays) and those resistant isolates may be correlated with molecular markers, many of which are based upon previous studies (Koernraadt et al 1992;Albertini et al 1999;Schnabel and Jones, 1991;Lesniak et al 2011). In some instances, segregation analysis between crosses of sensitive and resistance phenotypes is often used to strengthen this correlation (Faretra and Pollastro 1993;Orth et al 1995;Dyer et al, 2000); however, the ultimate mechanism of resistance is often lacking.…”