HETHERINGTON, FLORA,MARY (2018) The response of Arabidopsis to low potassium availability. Doctoral thesis, Durham University.
|PDF - Accepted Version|
The potassium ion (K+) is vital for plant growth and development, and K+ deficiency leads to reductions in crop yields. Given the significance of K+ deficiency in agriculture, it is important to understand the mechanisms by which K+ is taken into the plant and also how K+ deficiency impacts on the architecture of the root system, both of which will influence the ability of the crop to forage for K+ in the soil. The overall objective of the work described in this thesis is to uncover the mechanisms by which plant hormones control the root architectural responses to low K+ in the Arabidopsis accession Col-0. This question has been investigated using a combination of microscopy, genetics, chemical intervention, transcriptomics and analysis of the published literature.
In response to low K+ Arabidopsis reduces its lateral root (LR) growth, and it was established that this reduction in growth is mediated through a reduction in cell division in the LR meristems. Analysis of RNA-Seq data allowed the identification of gene transcriptional changes in response to low K+. These data were then used to form hypotheses about the hormonal control of the reduction in LR growth. Data in this thesis allowed the identification of a role for the hormone gibberellin (GA) and for DELLA proteins in the modulation of LR growth in response to K+ starvation. These data were also used to identify the CBF1 transcription factor as a potential regulator of changes in cellular GA levels in response to low K+. The roles of reactive oxygen species (ROS), ethylene, auxin and abscisic acid (ABA) in the regulation of the root architectural responses to low K+ were investigated but no clear regulatory effects were identified. A role for ethylene and low K+ in the root gravitropic response was also identified. A model is proposed that describes the link between low K+ availability and root architectural changes mediated by altered GA signalling pathways.
|Item Type:||Thesis (Doctoral)|
|Award:||Doctor of Philosophy|
|Faculty and Department:||Faculty of Science > Biological and Biomedical Sciences, School of|
|Copyright:||Copyright of this thesis is held by the author|
|Deposited On:||16 Jan 2018 13:21|