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Title: The role of auxin in host responses during cauliflower mosaic virus infection
Author: Smith, Lorna Ann
ISNI:       0000 0001 3449 3323
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 2006
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The role of auxin in the host response during compatible virus infection was examined in Arabidopsis with Cauliflower mosaic virus (CaMV). A genetic approach was adopted and a number of auxin signalling and transport mutants were used. The host responses including, symptom type and severity, virus movement and virus titre were not affected by disruptions to auxin signalling conferred by mutations of the AUX1 influx carrier or by mutations in TIR1 or TIR2. The tir3-1 mutation which contains a mutation in TIR3 locus which is involved in the synthesis, localisation and functioning of the NPA binding site within the efflux carrier as well as protein trafficking did show an altered response to infection. tir3-1 plants showed a consistent delay in the development of symptoms as well as delayed and reduced virus titre and viral spread. Virus infection up-regulated the expression of a number of auxin responsive genes, SAG21, SAUR_e and GH3. This upregulation was significantly reduced in aux1-100 and tir3-1 mutants. The expression of another auxin responsive gene LAX2 was found to be reduced in response to infection. From these findings it would appear that auxin signalling and transport is involved in some way during the infection process. Auxin levels were quantified in the AUX1 mutant allele aux1-100 and the wild type WS. No differences in levels of free IAA were observed. A synthetic auxin response element was also examined using both GUS and GFP reporters but again no alterations in auxin could be found. This could be due to the changes in auxin concentration being very subtle and therefore the techniques used failed to identify these changes, or it could be that the virus is interacting with specific components of the auxin signalling and transport pathways and the auxin responses are as a consequence of this rather than direct changes in auxin levels. One CaMV gene product which may be interacting with the auxin pathway is P6. Previous studies have shown that P6 is responsible for symptom determination and host response and that it interacts with other signalling pathways including the ethylene and SA pathways. It has been found here that P6 conferes resistance to the auxin efflux inhibitor TIBA and that it increases the expression of the auxin responsive gene SAUR_e. This resistance is independent of the chlorosis and stunting associated with P6. Preliminary genetic analysis of this interaction has idendified an interaction between tir3-1 and P6. Progeny of crosses between tir3-1 mutants and the P6 transgenic Arabidopsis line A7 show an aberrnat segregation ratio which suggests that tir3-l is able to suppress the P6 phenotype. These results suggest that a specific component of the auxin signalling pathway is involved in the host response to compatible infection. It is possible that P6 interacts directly with TIR3 rather than altering IAA levels. TIR3 is involved in protein trafficking and therefore could be a requirement for successful infection. Alterations in this gene could affect the trafficking of auxin signalling components such as PIN1 and lead indirectly to the auxin responses seen during infection.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral