|Secor, Gary -|
|Rivera, Viviana -|
|Birla, Keshav -|
Submitted to: Journal of Sugar Beet Research
Publication Type: Abstract Only
Publication Acceptance Date: October 22, 2010
Publication Date: June 1, 2011
Citation: Bolton, M.D., Secor, G.A., Rivera, V.V., Birla, K. 2011. Mechanism of DMI resistance in field isolates of Cercospora beticola [abstract.] Journal of Sugar Beet Research. 48:94. Technical Abstract: Leaf spot, caused by the fungus Cercospora beticola, is an endemic disease of sugarbeets in the North Dakota and Minnesota growing regions. Control measures against the fungus include resistant sugarbeet varieties and crop rotation, but the disease is managed effectively only when combined with timely fungicide applications. However, C. beticola is well-known for the ability to develop resistance to fungicides of several chemical classes. Previous research has shown that mutation in specific genes allow fungi to develop resistance to sterol demethylation inhibitor (DMI) fungicides, which are widely used to control leaf spot disease. DMI fungicides target an enzyme called 14 –demethylase (CYP51). Resistance to DMI fungicides has been shown to relate to specific mutation in the CYP51 gene, which causes decreased affinity of DMIs to the target enzyme or over-expression of the CYP51 gene leading to an over-production of the target enzyme. The objectives of this research were to determine if reduced sensitivity to DMI fungicides in C. beticola can be attributed to these or other known mechanisms of DMI resistance in other fungi. Single spore isolate cultures were derived from field isolates and fungicide EC50 vales to several DMI fungicides were obtained. The full-length CYP51 gene was cloned and sequence analysis was carried out to test whether specific mutations in the gene correlate with EC50 values. Results from these on-going investigations will be presented.