Poster: Biology & Disease Mgmt: Chemical Control
Induced overexpression of the gene MfCYP51 may reveal molecular mechanisms associated to tebuconazole resistance of Monilinia fructicola in Brazil.
P. LICHTEMBERG (1), Y. Luo (1), T. Michailides (1), L. May De Mio (2) (1) University of California - Davis, U.S.A.; (2) Universidade Federal do Paraná, Brazil
The aim of this study was to investigate the mechanism associated with Monilinia fructicola resistance to demethylation inhibitor fungicide (DMI) tebuconazole in Brazil. In this study 10 isolates (8 DMI-R and 2 DMI-S) with broad tebuconazole sensitivity (0,003 - >10 µg/ml) were used to quantify the expression levels of the genes MfCYP51 and MfABC1, respectively encoding the target enzyme 14 α-demethylase and mediating the transport of substances across biological membrane. After the mycelial exposure to sub-lethal doses of tebuconazole, the 2-ΔΔCt method revealed increased MfCYP51 mRNA levels for 6 out of 7 DMI-R isolates (ranging from 1.06 to 9.08), while DMI-S revealed small expressions levels of 0.14 and 0.46. The induced expression of the MfABC1 gene with tebuconazole on isolate mycelium not always increased the levels of mRNA. The Mona element which likely trigger the elevated expression of MfCYP51 was not present on 58 DMI-R isolates from Brazil including those with increased expression, suggesting that other genetic change yet to be discovered may be triggering this mechanism. Full MfCYP51 sequencing is currently underway. This is the first report on molecular mechanisms for DMI resistance identification for M. fructicola isolates from Brazil; providing an important advancement for risk assessment of DMI fungicides used on brown rot management.