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A bioinformatic analysis of genes involved in stress responses in Arabidopsis thaliana

By Linda Karen Hughes

Abstract

Hyaloperonospora arabidopsidis is an obligate biotrophic oomycete shown to cause\ud downy mildew in Arabidopsis thaliana. The main focus of this project is examining\ud plant stress response and the strategies employed by H. arabidopsidis to infect\ud Arabidopsis and evade plant stress responses. Two regions of the H. arabidopsidis\ud genome containing genes expressed in planta during infection were bioinformatically\ud annotated. The results indicated the genes were involved in regulatory processes\ud associated with the pathogenicity of H. arabidopsidis but not a direct role in\ud pathogenicity. H. arabidopsidis infects its host by secreting effector proteins into the\ud cytoplasm and apoplastic space of the host. The secretome of H. arabidopsidis was\ud analysed to identify classes of cysteine rich apoplastic effectors. This identified 15\ud candidate elicitin (ELI) and elicitin-like (ELL) sequences, three Kazal-like serine\ud protease inhibitors and four candidates similar to the protein sequences of Ppats 14\ud and 24, expressed during infection.\ud A second set of aims was to identify potential signalling networks up activated\ud during plant defence responses to infection by H. arabidopsidis using a new model\ud developed by Beal et al (Beal, Falciani et al. 2005) to eventually engineer\ud transcriptional networks. Unfortunately this failed due to problems with the\ud experiment. However, it was still possible to identify signalling networks from a\ud second microarray time course experimental data set centred on signalling networks\ud up regulated in response to the onset of senescence, as they share overlapping\ud signalling pathways. The modelling methodology was used to model the\ud anthocyanin biosynthesis pathway. The model predicted the presence of AtMYB15\ud as a positive regulator of anthocyanin biosynthesis along with AtMYB90. Research\ud carried out by Nichola Warner (Warner 2008) suggested that AtMYB90 was not\ud essential for anthocyanin biosynthesis during senescence based on by comparing the\ud phenotype of the MYB90 knock out, IM28, with the wild type (WT) Col-0 using a\ud time course microarray. Models of networks of transcriptional regulation of the\ud anthocyanin biosynthesis pathway for IM28 and WT implicate AtMYB29 as a\ud positive regulator of anthocyanin biosynthesis

Topics: QK
OAI identifier: oai:wrap.warwick.ac.uk:3729

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