UVM Theses and Dissertations
Format:
Print
Author:
Duncan, Zhen
Dept./Program:
Plant Biology
Year:
2010
Degree:
MS
Abstract:
The existence in Arabidopsis thaliana ofNIM1/NPRl-independent resistance has been well-documented. To identify signaling components in NIM1/NPR1-independent pathways that provide resistance to an oomycete pathogen, genetic screens were performed in a nim1 mutant background to look for additional mutations that result in increased susceptibility to an incompatible Hyaloperonospora arabidopsidis isolate, Noco2. A novel gene NIP1, (NIM1/NPR1-independent resistance to Peronospora) was previously identified and partially characterized.
In this thesis, I described the results of additional phenotypic and molecular analysis of nip1mutants, as well as higher resolution genetic mapping of the NIP1 gene. I showed that nip1 mutants displayed increased susceptibility to both avirulent and virulent strains of H. arabidopsidis. The increased susceptibility phenotype to the virulent strain of Ha. Emwal can be countered by INA application, indicating an intact systemic acquired resistance response. Gene expression profiles indicated that mRNA accumulation levels of RPP1-A, RPP1-B, and RPP1-C genes were not dramatically affected in nipi mutants. However, the expression leyels ofthe defense signaling genes EDSI and PAD4 were partially suppressed.
Three different mapping strategies were described with the goal of localizing the NIP1 gene to a precise location, permitting its positional cloning. Currently, the genetic interval containing NIP1 has been narrowed down to a 2.6 cM region between markers PERL0628 and BKN7322 on chromosome III. The subsequent successful cloning of the NIP1 gene will help us gain more understanding of its function in regulating NIM1/NPR1-independent disease resistance.
In this thesis, I described the results of additional phenotypic and molecular analysis of nip1mutants, as well as higher resolution genetic mapping of the NIP1 gene. I showed that nip1 mutants displayed increased susceptibility to both avirulent and virulent strains of H. arabidopsidis. The increased susceptibility phenotype to the virulent strain of Ha. Emwal can be countered by INA application, indicating an intact systemic acquired resistance response. Gene expression profiles indicated that mRNA accumulation levels of RPP1-A, RPP1-B, and RPP1-C genes were not dramatically affected in nipi mutants. However, the expression leyels ofthe defense signaling genes EDSI and PAD4 were partially suppressed.
Three different mapping strategies were described with the goal of localizing the NIP1 gene to a precise location, permitting its positional cloning. Currently, the genetic interval containing NIP1 has been narrowed down to a 2.6 cM region between markers PERL0628 and BKN7322 on chromosome III. The subsequent successful cloning of the NIP1 gene will help us gain more understanding of its function in regulating NIM1/NPR1-independent disease resistance.