Living in the Shadows: How Plants Balance Growth and Jasmonate-Dependent Defense Responses in the Shade.

No wonder the plants in my vegetable garden come down with every disease known to the plant kingdom; they don’t get enough sun! Shady conditions trigger a suite of responses that are all too familiar, including stem and petiole elongation, upward bending of leaves, early flowering, and reduced disease resistance. In the forest, the red/far red (R/FR) light ratio decreases due to the absorption of R light by plants in the canopy layer. In the understory, this light shift is detected by photoreceptors such as phytochrome B (phyB), causing these plants to ratchet up their growth in an attempt to outcompete their neighbors, which leaves fewer resources available for defense. However, since disease vectors lurk in shady as well as sunny locations, this balance of resources has to be finely tuned. Many plant defense responses are mediated by the phytohormone jasmonate (JA). Inactivation of phyB by low R/FR ratios somehow promotes a reduction in the plant’s sensitivity to JA and JA-dependent defense gene expression, lowering its resistance to insect herbivory and necrotrophic pathogens (deWit et al., 2013). However, the molecular mechanism underlying the complex response of plants to shade conditions remains unclear. Several transcription factors (TFs) that activate various JA-mediated responses have been identified, including MYC2, MYC3, and MYC4. Under basal conditions, JAZ repressors block the activity of these TFs, while increased JA levels lead to the degradation of JAZ repressors by the 26S proteasome. This, in turn, activates theMYC TFs, unleashing JA-mediated responses. Such responses are only now coming into focus. For example, Fernández-Calvo et al. (2011) showed that MYC2, MYC3, and MYC4 are involved in the activation of JAmediated defense responses to herbivory. Chico et al. (pages 1967–1980) go one step further, showing that these TFs are also required for JA-mediated defenses against the necrotrophic pathogen Botrytis cinerea. In this important study, the authors also uncover a mechanism underlying the regulation of these TFs and their JAZ repressors by light quality, bridging the gap in our understanding of how shade represses JAmediated disease resistance. The authors analyzed the expression of MYC2, MYC3, and MYC4 fused to green fluorescent protein in transgenic Arabidopsis thaliana plants in the presence of a translational inhibitor, revealing that these TFs are short-lived and regulated through proteasomal degradation. JA stabilizes these proteins, while dark and FR treatment lead to their degradation; JA treatment only partially restores this dark-induced destabilization. In addition, mutant analysis indicated that light-activated phyB is required for MYC2 stability. Moreover, while wild-type plants exhibit increased susceptibility to B. cinerea in simulated shade, as expected, the myc2 myc3 myc4 mutant is susceptible to this pathogen under both white light and shade conditions (see figure). Therefore, MYC2, MYC3, and MYC4 mediate JA-mediated defenses against B. cinerea, and shadetriggered susceptibility is likely achieved by FR-mediated inactivation of these TFs. In the shade, although pathogen attack triggers the production of JA, plants only partially regain their ability to fight back, as the restoration of the MYC TFs is limited, and plant defenses are therefore weakened. The authors also determined that simulated shade increases the abundance of JAZ repressors, adding another detail to the complex molecular mechanism underlying the shade response and giving me another reason to grow ferns instead of shade-intolerant vegetables.