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dc.contributor.advisorShuai, Bin
dc.contributor.authorDoerksen, Tyler
dc.date.accessioned2013-02-27T18:13:41Z
dc.date.available2013-02-27T18:13:41Z
dc.date.copyright2012en
dc.date.issued2012-07
dc.identifier.othert12055
dc.identifier.urihttp://hdl.handle.net/10057/5527
dc.descriptionThesis (M.S.)--Wichita State University, College of Liberal Arts and Sciences, Dept. of Biologyen_US
dc.description.abstractMacrophomina 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.en_US
dc.format.extentx, 46en
dc.language.isoen_USen_US
dc.publisherWichita State Universityen_US
dc.rights©Copyright 2012 by Tyler Doerksen. All Rights Reserveden
dc.subject.lcshElectronic dissertationsen
dc.titleInvestigating the genetic variations among Medicago truncatula ecotypes in response to pathogenic fungus Macrophomina phaseolinaen_US
dc.typeThesisen_US


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  • BIO Theses [67]
  • LAS Theses and Dissertations [665]
    Theses and dissertations completed at the College of Liberal Arts and Sciences (Fall 2005 -)
  • Master's Theses [1407]
    This collection includes Master's theses completed at the Wichita State University Graduate School (Fall 2005 --)

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