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Gordon Research Conference Plant Cell Walls 2012 – Cell Wall Research in a Post-Genome World, Waterville, USA 5th – 10th August 2012
The Gordon Research Conference on Plant Cell Walls, held triannually since 1997, brings together international plant cell wall specialists for a discussion of the state-of-the-art of the field.
Like all GRCs, it is an intimate and intense meeting with talks from morning to lunch time, followed by poster sessions in the afternoon and then more talks after dinner. All participants are lodging together and sharing their meals to foster the kind of communicative, focussed atmosphere that is the ideal of any scientific meeting. The remote Colby College in Waterville, Maine . mostly empty during term break – provided a great venue for the 5-day program, which was attended by approximately 200 participants and thus relatively large for a GRC.
Given the current focus on biofuels, naturally a large part of this cell wall meeting was centred around the use of cellulose and other wall polysaccharides in energy production. Prof Chris Somerville, director of the Energy Biosciences Institute (Berkeley, USA), presented the current state of this research in his opening plenary lecture. He highlighted that transport and engineering problems are at the core of current limitations to the utility of cellulosic biofuels and biologists therefore need to engage more strongly with process engineers and industrial chemists to make progress.
Besides its obvious importance for some of the most pressing questions facing industrialised societies today, the plant cell wall is also the main barrier that all plant pathogens have to penetrate at some stage of their infection, even if their life cycle occurs in the apoplast. It is the contributions that focussed on this aspect of cell wall research which I have highlighted here for BSPP members.
An exciting area of work, where important new findings with close links to plant pathology are currently being made, is signalling between the cell wall and the inside of the cell. Dr Giulia De Lorenzo from the University of Rome described work in her lab on the sensing of oligogalacturonans (OGs). OGs are damage associated molecular patterns (DAMPs) that result from partial degradation of homogalacturonan, a major component of pectin, for instance when a pathogen is digesting its way through the cell wall. Plant cells express polygalacturonase-inhibiting proteins (PGIPs), which are part of a pectin integrity monitoring system (PIMS) and slow down pathogen-derived endopolygalacturonases.
This not only protects the cell wall directly, but also boosts the accumulation of elicitor-active OGs with . 9 galacturonosyl residues. The De Lorenzo lab has recently shown that OGs are perceived through the wallassociated kinase WAK1, and downstream signalling proceeds via the MAP kinase MPK6. Dr De Lorenzo presented new crop protection strategies based on these results: Overexpression of PGIPs can confer or increase plant resistance against various pathogens and together with her colleagues, her lab used this strategy successfully to protect solanaceous species not only against fungi (Botrytis), but also for the first time against oomycetes (Phytophtora). Another promising approach currently under investigation in the De Lorenzo lab is the overexpression of WAK1 or the expression of WAK1-chimeric receptors to broaden the disease resistances of crop plants.
Another interesting contribution in this area was made by Dr Julia Davies (University of Cambridge), who talked about the role of apoplastic nucleotides in plant signalling. Extracellular (e)ATP and eADP regulate several cellular processes in plants, including growth, stomatal aperture and stress and pathogen responses. In particular, eATP is depleted during fungal elicitor-induced cell death and its ectopic application can reverse the apoptotic process. ATP and ADP are released into the apoplast by ABC transporters, and removed by apoplastic apyrases, however plants lack homologues of animal purinoceptors and it remains unclear how eATP/eADP are perceived. The Davies lab had previously shown that both eATP and eADP elicit Ca2+ fluxes into protoplasts, i. e. must be perceived at the plasma membrane rather than in the cell wall. eATP, but not eADP causes an increase in reactive oxygen species (ROS) via a plasma membrane NADPH oxidase, which in turn activate Ca2+ channels. Now, the lab has identified Annexin1 (ANN1), an apoplastic protein that can bind and insert into the plasma membrane, as the putative ROS-activated Ca2+ channel acting downstream of eATP. Reconstituted ANN1 can produce a Ca2+ conductance in artificial bilayers in response to hydroxyl radicals, and the ann1 loss-of-function mutant lacks ROS -activated Ca2+ influxes.
In my own talk, I presented an overview of current ideas of the structure of plasmodesmata (PD), the intercellular nanopores connecting plant cells across the wall. PD are of course the only pathway available to plant viruses for cell-to-cell movement. However, they are also increasingly emerging as signalling hubs in all kinds of pathogen responses. The membranes within PD channels – the plasma membrane surrounding the channel, and the central strand of endoplasmic reticulum – are probably highly specialised membrane domains and the PD plasma membrane in particular may be enriched in lipid raft-like assemblies, which are frequently associated with signalling events. In line with this view, PD have been found to contain receptor-like kinases (e.g. CR4) and the PDLP (PD localised protein) family of receptor-like proteins, which are implicated in responses against bacteria and herbivory, as well as being hijacked by viruses as PD receptors. (In the meantime, several additional examples of PD functioning as defence signalling hubs have been published).
In conclusion, I would like to thank the organisers for inviting me to speak at the conference, and the BSPP for the support with the travel costs. The 2012 GRC Plant Cell Wall conference was a very successful meeting, so successful indeed that it will be held biannually from now on. I certainly learned a great deal and left with the strong impression that there is a great deal that plant pathologists and plant cell wall biologists can learn from each other.
Jens Tilsner University of St Andrews and James Hutton Institute