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dc.contributor.advisorTar’an, Bunyaminen_US
dc.creatorThompson, Courtneyen_US
dc.date.accessioned2014-01-21T12:00:10Z
dc.date.available2014-01-21T12:00:10Z
dc.date.created2013-12en_US
dc.date.issued2014-01-20en_US
dc.date.submittedDecember 2013en_US
dc.identifier.urihttp://hdl.handle.net/10388/ETD-2013-12-1343en_US
dc.description.abstractWeed control in chickpea (Cicer arietinum L.) is challenging because of poor crop competition ability and limited herbicide options. Development of chickpea varieties with resistance to different herbicide modes of action would be desirable. Resistance to imidazolinone (IMI) herbicides in chickpea has been previously identified, but the genetic inheritance and the mechanism were unknown. In many plant species, IMI resistance is caused by point mutation(s) in the acetohydroxyacid synthase (AHAS) gene resulting in an amino acid substitution. This changes the enzyme configuration at the herbicide binding site, preventing the herbicide attachment to the molecule. The main research objective was to genetically characterize chickpea resistance to imidazolinone herbicides. Two homologous AHAS genes, namely AHAS1 and AHAS2 sharing 80% similarity were identified in the chickpea genome. A point mutation in AHAS1 at cytosine 675 thymine 675 resulting in an amino acid substitution from alanine 205 to valine 205 confers the resistance to imidazolinone in chickpea. A KASP marker targeting the point mutation was developed and effectively predicted the herbicide response in the RIL population. This same population was used in molecular mapping where the major locus for herbicide resistance was mapped to chromosome 5. Segregation analysis demonstrated that the resistance is inherited as a single gene in a semi-dominant fashion. To study the synteny of AHAS across plant species, lentil (Lens culinaris) AHAS1 was sequenced. The same mutation that confers the resistance to imidazolinone in chickpea was also found in lentil. Phylogenetic analysis indicated independent clustering of AHAS1 and AHAS2 across pulse species. In vivo and in vitro AHAS enzyme activity analysis showed inhibition of AHAS activity in the susceptible genotype CDC Frontier over time and with the increasing imidazolinone concentrations. In contrast, the resistant genotype CDC Cory did not show AHAS inhibition under the same treatments. In summary, the simple genetic inheritance and the availability of KASP marker could aid in the development of chickpea varieties with resistance to imidazolinone herbicide.en_US
dc.language.isoengen_US
dc.subjectchickpea, imidazoline, herbicide resistance, gene mapping, marker assisted selectionen_US
dc.titleGenetic characterization of the acetohydroxyacid synthase (AHAS) gene responsible for imidazolinone resistance in chickpea (Cicer arietinum L.).en_US
thesis.degree.departmentPlant Sciencesen_US
thesis.degree.disciplinePlant Scienceen_US
thesis.degree.grantorUniversity of Saskatchewanen_US
thesis.degree.levelMastersen_US
thesis.degree.nameMaster of Science (M.Sc.)en_US
dc.type.materialtexten_US
dc.type.genreThesisen_US
dc.contributor.committeeMemberCoulman, Bruceen_US
dc.contributor.committeeMemberBeattie, Aaronen_US
dc.contributor.committeeMemberWillenborg, Chrisen_US
dc.contributor.committeeMemberXiao Qiu, Xiaoen_US


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