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Genetic dissection of phytochrome A signal transduction in Arabidopsis

The signalling pathway of phytochrome A (phyA) is complex. This thesis describes analysis of mutants with altered phyA-mediated responses for enhancement of understanding concerning phyA signalling. A novel Arabidopsis mutant ( gil1) has been isolated which defines a point of interaction between phytochrome signalling and gravity signalling. This mutant, in contrast to wild-type (wt), displays gravitropic orientation of hypocotyls under red (R) and far-red (FR) light. The phytochrome mediated agravitropism, observed in wt under R and FR, is mediated by phyA and phytochrome B (phyB). Analysis of the gil1 mutant phenotypes suggests that this mutant is impaired in both phyA and phyB mediation of agravitropism. The T-DNA insertion, which is most likely responsible for the phenotype associated with gil1, was located to chromosome V, between two genes predicted by sequence analysis. Reduced expression of one of these genes (K19M22.14) occurs in gil1. Database analysis of the sequence of the K19M22.14 gene suggests no homology to any recognised genes. The phyA signalling mutant fhy3 has diminished responses to FR but amplified responses to R. The phenotypes associated with these amplified responses to R are here characterised for a number of different alleles in three ecotypes of Arabidopsis. Results suggest that fhy3 has some enhanced responses to R, and that these are more apparent in some alleles/ecotypes. Analysis of the fhy3phyB double mutant indicates that phyB is required for the enhancement of R responses through FHY3. Isolation and preliminary characterisation of mutants (sofs) which suppress some phenotypes of fhy1 is presented. These mutants may define new components of the phyA signalling pathway.

Identiferoai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:696786
Date January 2000
CreatorsAllen, Trudie
PublisherUniversity of Leicester
Source SetsEthos UK
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation
Sourcehttp://hdl.handle.net/2381/29821

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