The John Innes Centre Publications Repository contains details of all publications resulting from our researchers.
The repository also includes Open Access publications, which can be identified by the icons found on search results.
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The creation of this publications repository was funded by BBSRC.
Arabidopsis downy mildew effector HaRxL106 suppresses plant immunity by binding to RADICAL-INDUCED CELL DEATH1.
New Phytologist (220) 232-248
Publisher's version: 10.1111/nph.15277
ID: 59594read more
The oomycete pathogen Hyaloperonospora arabidopsidis (Hpa) causes downy mildew disease on Arabidopsis. To colonize its host, Hpa translocates effector proteins that suppress plant immunity into infected host cells. Here, we investigate the relevance of the interaction between one of these effectors, HaRxL106, and Arabidopsis RADICAL-INDUCED CELL DEATH1 (RCD1). We use pathogen infection assays as well as molecular and biochemical analyses to test the hypothesis that HaRxL106 manipulates RCD1 to attenuate transcriptional activation of defense genes. We report that HaRxL106 suppresses transcriptional activation of salicylic acid (SA)-induced defense genes and alters plant growth responses to light. HaRxL106-mediated suppression of immunity is abolished in RCD1 loss-of-function mutants. We report that RCD1-type proteins are phosphorylated, and we identified Mut9-like kinases (MLKs), which function as phosphoregulatory nodes at the level of photoreceptors, as RCD1-interacting proteins. An mlk1,3,4 triple mutant exhibits stronger SA-induced defense marker gene expression compared with wild-type plants, suggesting that MLKs also affect transcriptional regulation of SA signaling. Based on the combined evidence, we hypothesize that nuclear RCD1/MLK complexes act as signaling nodes that integrate information from environmental cues and pathogen sensors, and that the Arabidopsis downy mildew pathogen targets RCD1 to prevent activation of plant immunity.
Trends in Plant Science (23) 822-832
Publisher's version: 10.1016/j.tplants.2018.06.003
ID: 59627read more
The mechanism of stomatal function (control of gas flux through the plant surface via regulation of pore size) is fundamentally mechanical. The material properties of the pore-forming guard cells must play a key role in setting the dynamics and degree of stomatal opening/closure, but our understanding of the molecular players involved and resultant mechanical performance has remained limited. The application of indentation techniques and computational modelling, combined with molecular tools for imaging and manipulating guard cells and their constituent cell walls, has opened the way to a systems approach to analysing this problem. The outcomes of these investigations have led to a reassessment of accepted paradigms and are providing a new understanding of the mechanism of stomatal mechanics.
Annual Review of Genetics
Publisher's version: 10.1146/annurev-genet-120417-031237
ID: 59656read more
In bacteria, more than half of the genes in the genome are organized in operons. In contrast, in eukaryotes, functionally related genes are usually dispersed across the genome. There are, however, numerous examples of functional clusters of nonhomologous genes for metabolic pathways in fungi and plants. Despite superficial similarities with operons (physical clustering, coordinate regulation), these clusters have not usually originated by horizontal gene transfer from bacteria, and (unlike operons) the genes are typically transcribed separately rather than as a single polycistronic message. This clustering phenomenon raises intriguing questions about the origins of clustered metabolic pathways in eukaryotes and the significance of clustering for pathway function. Here we review metabolic gene clusters from fungi and plants, highlight commonalities and differences, and consider how these clusters form and are regulated. We also identify opportunities for future research in the areas of large-scale genomics, synthetic biology, and experimental evolution. Expected final online publication date for the Annual Review of Genetics Volume 52 is November 23, 2018. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.