Date of Award

5-31-2016

Document Type

Campus Access Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Biology/Molecular, Cellular, and Organismal Biology

First Advisor

Adán Colón-Carmona

Second Advisor

Michael Shiaris

Third Advisor

Rick Kesseli

Abstract

Ubiquitous organic pollutants polycyclic aromatic hydrocarbons (PAHs) consisting of two or more benzene rings are highly persistent in the environment. PAHs are derivatives of petroleum-based manufacturing and are released into the environment such as during incomplete combustion, by-products in chemical manufacturing and through oil spills. PAHs have a broad impact on the overall health of plants and animals. In cells, PAHs are transformed by oxidases and reductases; and their metabolism generates reactive electrophilic metabolites. These reactive compounds generate oxidative stress and DNA damage, leading to cell death and/or mutations. Nevertheless, how PAHs signal oxidative stress and are detoxified by cells is poorly understood. To identify some of the molecular players in either the signaling or the biodegradation, we screened a large pool of plant mutant lines of Arabidopsis thaliana and identified a mutant that is tolerant to PAH exposure, specifically phenanthrene, a 3-ring PAH. We named the mutant phenanthrene resistant 1, phr1. The phr1 mutant is an over-expression line of CYP702A6 (At4g15396), a member of the CYP85 clan of cytochrome P450 (CYP450) superfamily. To verify the observed phenotype of phr1, recapitulation experiments with constitutively expressed CYP702A6/At4g15396 were carried out. An analysis of null mutants supported the observation that CYP702A6 expression is required for the PAH tolerance. In addition, overexpression of CYP702A6 resulted in an overall robust phenotype on phenanthrene relative to wild type plants. Most probably CYP702A6 is involved as a crucial element in the PAH stress response pathway by participating in the degradation pathway, regulating antioxidant concentrations, modifying hormone levels, and enhancing metabolic pathways that alleviate the PAH stress response. Overall, CYP702A6/PHR1 expression plays a major role in ameliorating the deleterious effects of PAH exposure.

Comments

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