Biotic stresses experienced by crops can result in a double blow to crop yield: the direct impact of pathogenic activity on the plant, but also, significantly, the detrimental effect of the plant’s own immunity-induced growth inhibition (Eichmann and Schäfer, 2015). It is increasingly being argued that this growth-immunity antagonism is not simply an inevitable result of sharing finite metabolic resources between multiple physiological processes, but is more likely due to underlying signalling networks being hardwired to suppress growth as a direct response to immunity or defence being triggered (Reitz et al., 2015; Kliebenstein, 2015; Eichmann and Schäfer, 2015). Elucidating in detail the elements involved in these shared signalling pathways and how they may be manipulated to uncouple immunity and growth inhibition is the overarching aim of my project.

Defence responses, including reactive oxygen species burst, mitogen activated protein kinase (MAPK) activation and defence gene expression, can be triggered in laboratory-grown Arabidopsis thaliana roots through the exogenous application of microbe- or pathogen-associated molecular patterns (MAMPs or PAMPs) such as flg22 (a 22 amino acid N-terminal portion of the bacterial flagellin protein (Chinchilla et al. 2007)), or through the exogenous application of endogenous damage-associated molecular patterns (DAMPs), such as Pep1 (Huffaker and Ryan 2007). Such treatment of A. thaliana roots has also been shown to cause significant root growth inhibition (as measured by primary root length). There is a growing interest in the potential involvement of cell cycle regulation.

My project aimed to:

1. Identify the effects of pattern-triggered immunity on cel cycle regulation and vice versa.

2. Employ novel transcriptomic techniques to identify cell cycle marker genes in the root meristem.

3. Elucidate possible mechanisms by which immunity may lead to cell cycle arrest.