Off-campus UMass Amherst users: To download campus access dissertations, please use the following link to log into our proxy server with your UMass Amherst user name and password.

Non-UMass Amherst users: Please talk to your librarian about requesting this dissertation through interlibrary loan.

Dissertations that have an embargo placed on them will not be available to anyone until the embargo expires.

Document Type

Campus-Only Access for Five (5) Years

Degree Name

Doctor of Philosophy (PhD)

Degree Program

Plant, Soil & Insect Sciences

Year Degree Awarded

2017

Month Degree Awarded

May

First Advisor

Geunhwa Jung

Subject Categories

Agricultural Science | Plant Pathology

Abstract

A filamentous ascomycete fungus Sclerotinia homoeocarpa causes dollar spot, which is the most important disease of turfgrasses in the United States. Despite the increased number of reports of site-specific fungicide resistance and a recent report of multidrug resistance (MDR) in S. homoeocarpa field populations, the genetic mechanisms behind resistance or reduced sensitivity to fungicides remain poorly explained in the fungus. In order to prevent further development of fungicide resistance in the dollar spot pathosystem, a detailed elucidation of mechanisms of site-specific fungicide resistance and MDR is needed. In addition, the previous studies of MDR in fungi mostly focused on efflux transporter mediated drug/xenobiotic detoxification. However, the recent release of fungal genome sequences has revealed that ascomycete filamentous fungi including S. homoeocarpa possess a large number of cytochrome p450s (CYP450s) that are involved in xenobiotic metabolism. Chapters 2 and 3 of this dissertation describe demethylation inhibitor (DMI) fungicide/MDR mechanisms in S. homoeocarpa through Phase I xenobiotic metabolizing enzymes (CYP450s) and Phase III efflux transporters using functional genomic and genetic techniques. We identified a fungal specific transcription factor (Shxdr1) that regulates the Phase I and III genes and a novel gain of function mutation of the transcription factor found from a MDR field strain is responsible for constitutive and induced overexpression of the Phase I and III genes, resulting in MDR. In Chapter 4, the mechanisms of qualitative and quantitative resistance of a dicarboximide fungicide have been determined using field and lab mutant S. homoeocarpa strains. We confirmed that S. homoeocarpa field isolates gained qualitative and quantitative dicarboximide resistance through the polymorphism in the histidine kinase gene Shos1 and the overexpression of ABC efflux transporter ShPDR1, respectively. Chapter 5 studies the management of a S. homoeocarpa population with different combinations of resistance to dicarboximide, DMI, and benzimidazole fungicides to find the best fungicide options for controlling the S. homoeocarpa population and further understanding the dynamics of how the population responds to fungicide applications, and to long-term lack of exposure to fungicides during winter. Succinate dehydrogenase inhibitors (SDHI; fluxapyroxad and boscalid (high rate)), multi-site fungicide (fluazinam), and the fungicide mixture (chlorothalonil, iprodione, thiophanate methyl, and tebuconazole) controlled the S. homoeocarpa population very well. The isolates with resistance to DMI and dicarboximide were most frequently selected by iprodione or propiconazole applications and the isolates with resistance to DMI and benzimidazole were selected by boscalid applications, but these multiple fungicide resistant isolates decreased after overwintering.

Available for download on Saturday, May 12, 2018

Share

COinS