The conference was very much a success. There was notable progress relative to the 2011 Asilomar meeting. Newcomers to the field gave their first OMGN talks and the presentations by local scientists illustrated the wide-range of research taking place in China. I was sorry to miss the closing dinner but I suppose I saved myself the embarrassment of participating in the Karaoke.
Below is an attempt to summarize and organize the somewhat random thoughts running through my head right now as I am sitting tight on the Shanghai to New York flight. Thanks to China Eastern Airlines for providing electrical outlets to all economy class passengers.
The hot topic: epigenetics - The talks by Wenbo Ma and Mark Gijzen were the most thought provoking for me. Many questions are racing through my head as I am revisiting Wenbo’s talk. To what extent do oomycete effectors suppress RNA silencing? Did they evolve to directly target RNA silencing machinery? What about the nuclear-localized CRNs? Dinah Qutob and Mark Gijzen’s findings also raise many questions. What proportion of Phytophthora genes are targeted by silencing? How frequently do epialleles emerge? How frequently do they revert? What I found particularly exciting about both presentations are the questions they provoke.
On the upswing: cell biology - Several presentations included a significant cell biology component but there is room for more. I expect cell biology to become increasingly integrated into oomycete research as we start considering the spatiotemporal aspects of the processes we study. As this happens we need to ensure that we use consistent standards and nomenclature.
Not much new: genomics - I did not pick up any obvious new trends in genomics. The loss of heterozygosity (LOH) phenomenon described in a poster by Kurt Lamour et al. is probably the main novelty. There were some new genomes, e.g. Saprolegnia parasitica, Pythium insidiosum, and Pseudoperonospora cubensis. But some of these were described to some extent at previous OMGN conferences. I felt the topic was less dominant than in the past. The talk by the BGI representative was disappointing.
What about apoplastic effectors? - How come so few are working on apoplastic effectors? None of the talks addressed these important players in oomycete-plant interactions.
Mechanisms of RXLR effector translocation: the plot thickens - There is definitely more clarity than one year ago but many questions remain. The C-terminal binding of AVR3a/AVR1b to PI3Ps described by Yaeno et al. (2011) has been confirmed by Tyler at al. At least this one aspect does not seem to be controversial. But even if AVR3a/AVR1b C-terminal binding to PIPs mediates host cell translocation, it cannot be a general mechanism given that the C-termini of other RXLR effectors do not bind PIPs (I think but I am not sure that this point is accepted by several groups). Kasturi Haldar had some useful advice by reminding us that there are multiple routes to host cell entry in plasmodia.
Is the RXLR leader generally involved in PIP binding? - A hotly debated issue remains the lack of reproducibility of the RXLR motif/domain binding to PIPs (Kale et al. 2010 vs. Yaeno et al. 2011 and unpublished reports). The first case of independent confirmation of this central finding of the Kale et al. paper is by Kasturi Haldar’s lab, which showed that the RXLR domain of P. infestans Nuk10 binds PI3Ps. However, the Haldar lab did not test the RXLR leader of AVR3a/AVR1b (pers. comm.), which are the leaders that could not be confirmed by Yaeno et al. and the van West lab (presented at OMGN11). Note also that the Nuk10 leader was not tested by Kale et al. Thus, in my view, the key finding of the Kale et al. paper - that the RXLR leader generally functions in PIP binding – still requires independent confirmation and would be nullified if indeed the AVR3a/AVR1b leader turns out to lack binding activity.
What about Kale et al. experiments with full-length effectors? - The validated finding that the C-termini of AVR1b and related effectors bind PIPs compromises a number of experiments described in the Kale et al. paper. Assays in which RXLR mutations in full-length effectors abolish PI3P binding, as well as translocation into cells and roots, are inconsistent with the strong PIP binding of the C-termini. This casts an additional shadow on the quality of the Kale et al. experiments, which have already been plagued by the duplicated figures issue and lack of reproducibility of key assays with the fungal “RXLR-like” sequences.
Other host-translocation leaders to the rescue? - Perhaps the breakthrough in understanding how oomycete effectors translocate inside host cells will come from other leaders than RXLR. Lobach, Wawra, van West et al. proposed that binding to tyrosine-O-sulphate on the host cell surface mediates entry of some Saprolegnia parasitica effectors. As far as I can tell this is not controversial although the finding has not been independently confirmed. Still, there is no work reported on other non-RXLR leaders, such as the Crinkler LxLFLAK and Albugo’s CHXC. Lets hope we’ll hear more about these in the future.
Pre-secretion sorting? - I was impressed by the talk of Zhijian Zhao, which I thought was the most interesting of the several talks by members of the Nanjing Agricultural University oomycete group. Zhijian is investigating how oomycete effectors are secreted, focusing on the pathogen side. We’ll surely hear more on this topic in the future.