Document Type



Meloidogyne incognita, a root-knot nematode (RKN), poses a threat to the well-being of the global agricultural industry. These endoparasites rely on plant roots and drain nutrients from crops intended for human or livestock consumption. Root knot nematodes cost the agricultural industry billions of dollars in lost crops each year and threaten efforts to meet the growing demand for food. Though plants are susceptible to dangers, such as these parasites, many have evolved defense and/or repair mechanisms to compensate for this vulnerability. The goal of this research is to study one gene family involved in such defenses. Specifically, I studied the effects of root-knot nematodes on JAZ gene expression in Arabidopsis thaliana. JAZ genes are the focus of this study due to their role as transcriptional regulators; however, it is uncertain if each gene has a distinct role or if they are interchangeable. To date, 13 JAZ genes have been identified in Arabidopsis and I focused on the roles of JAZ 1, 12, and 13 during root-knot nematode infection. In order to look at expression and localization of JAZ1 and JAZ12, I used promoter GUS lines to observe staining in the roots during nematode infection between six hours and twenty-seven days post infection. Staining was variable between transgenic lines and time points, though JAZ1::GUS A2 showed to be the most sensitive to RKN infection. To identify jaz1 mutant plants, I conducted PCR and visualized products via gel electrophoresis to ensure T-DNA insertion in the gene was successful. I then isolated a jaz1 mutant and tested it for nematode infection. Mutant seedlings were inoculated with RKN eggs and I compared the number of egg masses between the mutant and Columbia wild-type after 8 weeks of incubation. There was no significant difference between wild-type and jaz1 seedlings. This was followed by qPCR on JAZ 1, JAZ12, and JAZ13 genes to test their expression during nematode infection in both uninfected portions roots and root knots over various stages of infection. These results indicate that expression of JAZ1 and JAZ12 is highest around 13-14 days of infection, suggesting these two genes may work in combination to attempt to rid the host of the pathogen. These results differ from JAZ13 expression, which peaked at three weeks of infection, indicating its role takes place after JAZ1 and JAZ12 expression has peaked. The goal of this research is to contribute to existing JAZ/RKN data and eventually exploit host defense pathways, so that the agricultural industry may reduce nematicide use and better fulfill food demands of our global population.



Thesis Comittee

Dr. Heather Marella, Thesis Advisor

Dr. M. Caitlin Fisher-Reid, Committee Member

Dr. Kenneth Adams, Committee Member

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Original document was submitted as an Honors Program requirement. Copyright is held by the author.

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