This project is funded by a BBSRC grant as a collaboration with the Universities of Lancaster and Manchester. You will join a team of a post-doctoral researcher and two research technicians.
Crop- and pasture-level ozone (O3) concentrations are a threat to productivity. Global yield losses in 2030 are predicted to be from 4-26% for wheat, 9.5-19% for soybean, 2.5-8% for maize and worth up to US$35 billion. European crop losses are worth several billion Euros annually. The frequency of ozone "episodes" (when local conditions promote significant ozone elevation during the growing season) is set to increase. Ozone is deleterious to both vegetative and reproductive growth with severity depending on the sensitivity of the genotype. Entering through stomata, ozone reacts in the apoplast to form Reactive Oxygen Species (ROS) leading to reduced shoot (and root) growth, visible lesions and leaf abscission. Flowering, pollen vigour and grain development are also affected by ozone. Guard cell closure is promoted by ozone and light-induced opening is prevented, compromising C fixation. During drought, ozone can impair stomatal closure, causing deleterious water loss. Thus the combination of increasing O3 levels and water scarcity endangers plant productivity. How plants defend against O3 must be understood to combat this problem.
Transcriptome analyses of ozone-challenged Arabidopsis has shown effects on genes for protein turnover, redox regulation, anthocyanin synthesis, vesicle transport, cell wall modification, photosynthesis, and signalling. What early signals lead to this genome response? Ozone rapidly triggers a specific biphasic and transient increase in cytosolic free Ca2+ that acts as a second messenger in Arabidopsis seedlings. This calcium signature can be prevented by treatment with lanthanum as a calcium channel blocker, confirming the necessity of calcium entry. The plasma membrane calcium channel mediating ozone signalling is unknown. We have has discovered that Arabidopsis annexin 1 (ANN1) forms a plasma membrane Ca2+ channel that is activated by ROS. It is therefore a strong candidate for mediating O3-induced calcium signalling. In this project, you could examine the effects of annexin loss of function on cell-specific ozone-induced calcium signatures, examine the transcriptional response of mutants using microarray and qPCR, and study the impact of annexin loss of function on guard cell kinetics, cell death and productivity. The project can also encompass work on key grassland species.