| Summary: | Macrophomina phaseolina, an internationally distributed fungal pathogen, causes a disease known as “charcoal rot” (also known as dry-weather wilt and summer wilt) that clogs vascular tissue and produces yellow, wilted plants with visible fungal sclerotia. Primarily acting in dry, hot conditions, it inflicts extensive economic losses in Midwestern crops such as soybean, alfalfa, sorghum, and cotton. To better understand the molecular mechanisms of the disease a model pathosystem was established using Medicago truncatula to study host-pathogen interactions. 319 ectoypes of M. truncatula were screened using a root-dip method to identify potential variations in host susceptibility (either unusual susceptibility or resistance) to M. phaseolina in hopes of revealing naturally existing genetic variations that can lead to host resistance. In this screen, all ecotypes showed normal disease progression compared to a reference genotype, Jemalong A17. Previous study showed that treatment with jasmonic acid (JA) and ethylene (ET) confer increased resistance to A17 but not to R108, another widely used M. truncatula genotype. To test the hypothesis that the difference in disease progression in A17 and R108 after exogenous treatment with JA and ET was due to differential regulation of the JA/ET pathways in these genotypes, expression of genes representing the JA and ET pathways were compared in A17 and R108 after inoculation with M. phaseolina. The results showed that genes indicative of the JA pathway were induced both faster and stronger in A17 than in R108, and marker genes representing ET pathway were more strongly upregulated in A17 than in R108. Since many of the marker genes used in this study are related to fungal defense and considering that the JA and ET pathways regulate plant defense genes, including those with antifungal properties, it is likely that the varying induction of JA and ET pathways is involved in the different hormonal responses between A17 and R108 to M. phaseolina infection. Testing that hypothesis requires further study of how these marker genes respond to exogenous JA and/or ET treatment in A17 and R108. === Thesis (M.S.)--Wichita State University, College of Liberal Arts and Sciences, Dept. of Biology
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