Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680600
Title: Characterisation of the MAD and 17-4 branching regulators of Arabidopsis
Author: Taylor, Danielle J.
Awarding Body: University of York
Current Institution: University of York
Date of Award: 2013
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Abstract:
Aerial morphology in higher plants is highly variable and demonstrates the ability of plants to adapt to prevailing conditions. Regulation of shoot branching is a vital aspect of plant growth, controlling shoot system architecture. The phytohormones; auxin, cytokinin, and strigolactone are closely involved in the regulation of bud outgrowth, and therefore shot branching, and the mechanisms by which they do this are of great scientific interest. The MAX (MORE AXILLARY GROWTH) pathway in Arabidopsis consists of a series of genes involved in strigolactone biosynthesis and signalling. Mutations in these genes have been used to great effect to elucidate the manner of auxin-mediated inhibition of shoot branching via the MAX pathway. The purpose of this study was twofold: Firstly, to characterise plants heterozygous for the semi-dominant mad (more apical dominance) mutation, which suppresses the max1 branching phenotype and secondly, to characterise the 17-4 mutant, which displays an increased branching phenotype similar to that of max2. Various physiological and genetic techniques were applied to this end. MAD/mad is not a general mediator of strigolactone signalling as it only affects the max1 branching phenotype. MAD/mad partially restores wild-type branching to all of the max mutants, suggesting that it acts either downstream of, or in parallel to, MAX2. The MAD locus is within a 370kb region on the p-arm of At. Chromosome 3. Among the 230 genes in this region are three of considerable interest, MES17, SPY, and AT3G11130.1 all with the potential for a role in the regulation of bud outgrowth and therefore all potential candidates for the MAD gene. 17-4 was isolated in a screen looking for mutants with high levels of branching in low nitrate conditions, and has striking morphological similarity to the well characterised max2 mutant. Complementation testing showed that 17-4 was not one of the currently recognised max2 alleles. This does not rule 17-4 out as a novel allele of max2. Increased branching in 17-4 is probably a result of increased auxin transport capacity and resistance to auxin-mediated suppression of bud outgrowth. 17-4 is not involved in strigolactone biosynthesis but appears to be involved in strigolactone signalling.
Supervisor: Leyser, Ottoline ; Waites, Richard Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.680600  DOI: Not available
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