Although open stomata are necessary for plants to take up CO2 for photosynthesis, this also permits loss of precious water – by transpiration, the so-called necessary evil of photosynthesis. But, surely, nothing worse can be associated with stomata, can it? Well, closed stomata also act as a barrier to entry of harmful microbes, and they may close in response to a potential threat, which is a good thing. However, some would-be invaders have managed to circumvent this and keep stomata open, thereby facilitating their unwanted entry into the plant. Which is a neat enough trick in itself. But how they manage this feat has been further elucidated by Xiao-yu Zheng and colleagues and reveals the subtle molecular deception involved in infection by the bacterium Pseudomonas syringae (which infects more than 50 plant species and is a major cause of surface frost damage in plants). The microbe produces coronatine (COR), which the plant cannot distinguish from jasmonic acid isoleucine (JA) – which is part of the plant’s microbe defence system. So far, this sounds like a case of the bacterium ‘shooting itself in the foot’ by producing a compound that should work against its own pathogenic ambitions. Well, that’s where the really cunning part comes into play. JA is only one part of the plant defences, salicyclic acid (SA) is another and plays an important role but in a different defence pathway. Both JA and SA interact, depending on the type of microbial attack that is detected, but effectively in opposition to each other. JA is produced in response to attack by necrotrophs (that kill the plant cells); SA is made when biotrophs (which keep plant cells alive and harvest what they produce) attack. As a JA-mimic, COR results in the activation of several transcription factors (‘regulatory molecules’ that control gene expression) within the plant cells that suppress SA formation – which would otherwise promote stomatal closure – by affecting both SA biosynthesis and SA metabolism. Consequently, this ‘coronatine-induced stomatal reopening’ permits more of the ‘biotrophs-in-necrotrophs’ clothing’ to enter and invade the plant’s tissues. I know it’s wrong, but I just can’t help but admire this subtle pseudomonic subterfuge. (But how does the first one get in to manage this magnificent microbial molecular magic?). Seemingly, this type of behaviour is not restricted to prokaryotes; Ustilago maydis, the eukaryote fungus that causes economically damaging corn smut of maize, is also able to suppress the host’s pathogen invasion defences. As demonstrated by Armin Djamei et al., upon infection the biotrophic fungus releases a plethora of proteins, one of which – the enzyme chorismate mutase (Cmu1) – effects ‘metabolic priming’ of the infected cell (and adjacent cells), resulting eventually in reduced production of… SA.
About the author
Nigel is a botanist and full-time academic at Bath Spa University (Bath, near Bristol, UK). As News Editor for the Annals of Botany he contributes the monthly Plant Cuttings column to that august international botanical organ. His main goal is to inform (hopefully, in an educational, and entertaining way...) about plants and plant-people interactions.