Self-incompatibility (SI) is a genetic mechanism which prevents self-fertilisation via the recognition and rejection of ‘self’ pollen. In the self-incompatible species Papaver rhoeas L., rejection of incompatible pollen is achieved through interaction of the female and male S-determinants, PrsS and PrpS, respectively. This interaction results in a Ca\(^{2+}\)-dependent signalling cascade in the ‘self’ pollen, which mediates programmed cell death (PCD). To date, many downstream effects of SI signalling cascade have been identified, including actin depolymerization, the formation of actin foci, and the activation of caspase-like activities. Work presented in this thesis identified the involvement of Reactive Oxygen Species (ROS) and Nitric Oxide (NO) in the SI response, and the temporal and spatial patterns were characterized. Other studies identified SI-induced cytosolic acidification as a key step in SI. Moreover, investigation of the role of ROS, NO and H\(^+\) revealed that they all play a role in triggering key features of SI: actin foci formation and caspase-3-like activity. Other studies also provided the first evidence for vacuolar breakdown in SI in this species. Data presented also show the first documentation of SI-induced alterations in phospholipids. Together these data further our understanding of mechanisms involved in the complex SI signalling network.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:569741 |
| Date | January 2013 |
| Creators | Wilkins, Katie Anne |
| Publisher | University of Birmingham |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://etheses.bham.ac.uk//id/eprint/4109/ |
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