A plant-specific family of WRKY transcription factors regulates plant responses to pathogens and abiotic stresses. Here, we identify two insect-responsive WRKY genes in the native tobacco Nicotiana attenuata: WRKY3, whose transcripts accumulate in response to wounding, and WRKY6, whose wound responses are significantly amplified when fatty acidamino acid conjugates (FACs) in larval oral secretions are introduced into wounds during feeding. WRKY3 is required for WRKY6 elicitation, yet neither is elicited by treatment with the phytohormone wound signal jasmonic acid. Silencing either WRKY3 or WRKY6, or both, by stable transformation makes plants highly vulnerable to herbivores under glasshouse conditions and in their native habitat in the Great Basin Desert, Utah, as shown in three field seasons. This susceptibility is associated with impaired jasmonate (JA) accumulation and impairment of the direct (trypsin proteinase inhibitors) and indirect (volatiles) defenses that JA signaling mediates. The response to wounding and herbivore-specific signals (FACs) demonstrates that these WRKYs help plants to differentiate mechanical wounding from herbivore attack, mediating a plant's herbivore-specific defenses. Differences in responses to single and multiple elicitations indicate an important role of WRKY3 and WRKY6 in potentiating and/or sustaining active JA levels during continuous insect attack.
The human pathogenic yeast Candida albicans can cause an unusually broad range of infections reflecting a remarkable potential to adapt to various microniches within the human host. The exceptional adaptability of C. albicans is mediated by rapid alterations in gene expression in response to various environmental stimuli and this transcriptional flexibility can be monitored with tools such as microarrays. Using such technology it is possible to (1) capture a genome-wide portrait of the transcriptome that mirrors the environmental conditions, (2) identify known genes, signalling pathways and transcription factors involved in pathogenesis, (3) identify new patterns of gene expression and (4) identify previously uncharacterized genes that may be associated with infection. In this review, we describe the molecular dissection of three distinct stages of infections, covering both superficial and invasive disease, using in vitro, ex vivo and in vivo infection models and microarrays.
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