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Title: The molecular mechanisms underlying gall formation in Plasmodiophora brassicae infected Arabidopsis thaliana
Author: Akhtar, Serina Ann
ISNI:       0000 0004 5349 442X
Awarding Body: University of Sheffield
Current Institution: University of Sheffield
Date of Award: 2014
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Plasmodiophora brassicae is an obligate pathogen that causes clubroot disease. Infection occurs in plants of the Brassica genus including many economically important crops and the model organism A. thaliana. The disease results in a gall forming on infected root tissue. The gall is a consequence of extensive host cell division and expansion, additionally the disease leads to a disruption in cellular differentiation and organisation. The gall has a negative impact on shoot growth and leads to reductions in yields that can be up to 100 % in heavily infected fields. Currently there are no effective measures for the prevention or treatment of the disease. The A. thaliana mutant ein5-1 was shown to be tolerant to infection compared with wild-type, Col-0. ein5-1 showed a delay in gall formation of approximately 7days, which was found to be a consequence of both delayed host symptom and pathogen development. ein5 encodes an exoribonuclease involved in ethylene signalling and miRNA-mediated cleavage. The role of these two pathways in infection was explored in order to further understand the tolerance response of ein5-1. Examination of the ein2-1 mutant indicated that perturbations in ethylene signalling were not responsible for the tolerance response of ein5-1. The miRNA-biogenesis mutant, hen1-5, displayed a response to clubroot that was reminiscent of that seen in ein5-1 indicating a possibly role for miRNA-silencing in clubroot infection. A microarray analysis was conducted to examine changes in gene expression in Col-0 and ein5-1 during infection. The analysis suggested that infection in both Col-0 and ein5-1 impacted on gene expression in a similar manner. However, a role for salicylic acid and flavonoid related genes during infection of ein5-1 was suggested. Further to this it was hypothesised that alterations in secondary metabolite content may play a role in ein5-1 tolerance.
Supervisor: Rolfe, Stephen ; Fleming, Andrew ; Scholes, Julie Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available