Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.572096
Title: Rhizobial infection in nodulation
Author: Guan, Dian
Awarding Body: University of East Anglia
Current Institution: University of East Anglia
Date of Award: 2012
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Abstract:
Nodulation is a symbiosis between plants and bacteria called rhizobia which leads to the formation of a lateral organ called a nodule where nitrogen fixation occurs. Nodulation can be divided into two developmental programmes, rhizobial infection, and nodule organogenesis, both of which are required for nitrogen fixation. In my PhD studies, I focused on the study of rhizobial infection using the Medicago truncatula-Sinorhizobium meliloti model system. NIN is an important transcription factor in the nodulation signalling pathway that functions both in rhizobial infection and nodule organogenesis. Gene expression profiling of nin during rhizobial infection has enabled me to identify its potential downstream targets including several NIN-dependent infection-related genes and, surprisingly, genes involved in mycorrhization that are apparently repressed by NIN. The identification of these genes has provided insight into how NIN functions in rhizobial infection and revealed potential cross-talk between nodulation and mycorrhization pathways. In the course of this work I discovered two infection mutants. One of the mutants, cbs1, was cloned in collaboration with a colleague in the lab. It encodes a Cystathionine Beta-Synthase domain containing protein with a potential role in reactive oxygen species homeostasis. The other mutant, which I named knocks but can’t enter (kce), is blocked at an early stage of infection. I used conventional mapping and next-generation sequencing technologies to genetically map kce to a known rhizobial infection gene LIN. The kce mutant developed nodules with central rather than peripheral vascular bundles resembling nodules from the more ancient Frankia-actinorhizal symbiosis. Using kce and other infection mutants I demonstrate that this abnormal nodule architecture results from a failure of infection to reach the nodule cortex. Based on this finding, I predict that Nod factor activated signalling in the nodule cortex plays a role in determining nodule structure.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.572096  DOI: Not available
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