Marcelo L. Campos

Jasmonate-Triggered Plant Immunity

The plant hormone jasmonate (JA) exerts direct control over the production of chemical defense compounds that confer resistance to a remarkable spectrum of plant-associated organisms, ranging from microbial pathogens to vertebrate herbivores. The underlying mechanism of JA-triggered immunity (JATI) can be conceptualized as a multi-stage signal transduction cascade involving: i) pattern recognition receptors (PRRs) that couple the perception of danger signals to rapid synthesis of bioactive JA; ii) an evolutionarily conserved JA signaling module that links fluctuating JA levels to changes in the abundance of transcriptional repressor proteins; and iii) activation (de-repression) of transcription factors that orchestrate the expression of myriad chemical and morphological defense traits. Multiple negative feedback loops act in concert to restrain the duration and amplitude of defense responses, presumably to mitigate potential fitness costs of JATI. The convergence of diverse plant- and non-plant-derived signals on the core JA module indicates that JATI is a general response to perceived danger. However, the modular structure of JATI may accommodate attacker-specific defense responses through evolutionary innovation of PRRs (inputs) and defense traits (outputs). The efficacy of JATI as a defense strategy is highlighted by its capacity to shape natural populations of plant attackers, as well as the propensity of plant-associated organisms to subvert or otherwise manipulate JA signaling. As both a cellular hub for integrating informational cues from the environment and a common target of pathogen effectors, the core JA module provides a focal point for understanding immune system networks and the evolution of chemical diversity in the plant kingdom.

Rewiring of jasmonate and phytochrome B signalling uncouples plant growth-defense tradeoffs

Plants resist infection and herbivory with innate immune responses that are often associated with reduced growth. Despite the importance of growth-defense tradeoffs in shaping plant productivity in natural and agricultural ecosystems, the molecular mechanisms that link growth and immunity are poorly understood. Here, we demonstrate that growth-defense tradeoffs mediated by the hormone jasmonate are uncoupled in an Arabidopsis mutant (jazQ phyB) lacking a quintet of Jasmonate ZIM-domain transcriptional repressors and the photoreceptor phyB. Analysis of epistatic interactions between jazQ and phyB reveal that growth inhibition associated with enhanced anti-insect resistance is likely not caused by diversion of photoassimilates from growth to defense but rather by a conserved transcriptional network that is hardwired to attenuate growth upon activation of jasmonate signalling. The ability to unlock growth-defense tradeoffs through relief of transcription repression provides an approach to assemble functional plant traits in new and potentially useful ways.

Negative Feedback Control of Jasmonate Signaling by an Alternative Splice Variant of JAZ10

A transcriptional regulator generated by alternative splicing uses a cryptic binding site to negatively regulate bHLH-type transcription factors that promote jasmonate responses. The plant hormone jasmonate (JA) activates gene expression by promoting ubiquitin-dependent degradation of jasmonate ZIM domain (JAZ) transcriptional repressor proteins. A key feature of all JAZ proteins is the highly conserved Jas motif, which mediates both JAZ degradation and JAZ binding to the transcription factor MYC2. Rapid expression of JAZ genes in response to JA is thought to attenuate JA responses, but little is known about the mechanisms by which newly synthesized JAZ proteins exert repression in the presence of the hormone. Here, we show in Arabidopsis (Arabidopsis thaliana) that desensitization to JA is mediated by an alternative splice variant (JAZ10.4) of JAZ10 that lacks the Jas motif. Unbiased protein-protein interaction screens identified three related basic helix-loop-helix transcription factors (MYC2, MYC3, and MYC4) and the corepressor NINJA as JAZ10.4-binding partners. We show that the amino-terminal region of JAZ10.4 contains a cryptic MYC2-binding site that resembles the Jas motif and that the ZIM motif of JAZ10.4 functions as a transferable repressor domain whose activity is associated with the recruitment of NINJA. Functional studies showed that the expression of JAZ10.4 from the native JAZ10 promoter complemented the JA-hypersensitive phenotype of a jaz10 mutant. Moreover, treatment of these complemented lines with JA resulted in the rapid accumulation of JAZ10.4 protein. Our results provide an explanation for how the unique domain architecture of JAZ10.4 links transcription factors to a corepressor complex and suggest how JA-induced transcription and alternative splicing of JAZ10 premessenger RNA creates a regulatory circuit to attenuate JA responses.

The Role of Phytochrome in Stress Tolerance

It is well-documented that phytochromes can control plant growth and development from germination to flowering. Additionally, these photoreceptors have been shown to modulate both biotic and abiotic stress. This has led to a series of studies exploring the molecular and biochemical basis by which phytochromes modulate stresses, such as salinity, drought, high light or herbivory. Evidence for a role of phytrochromes in plant stress tolerance is explored and reviewed.

Repression of jasmonate signaling by a non-TIFY JAZ protein in Arabidopsis.

JAsmonate ZIM-domain (JAZ) proteins repress the activity of transcription factors that execute responses to the plant hormone jasmonoyl-L-isoleucine (JA-Ile). The ZIM protein domain recruits the co-repressors NINJA and TOPLESS to JAZ-bound transcription factors, and contains a highly conserved TIF[F/Y]XG motif that defines the larger family of TIFY proteins to which JAZs belong. Here, we report that diverse plant species contain genes encoding putative non-TIFY JAZ proteins, including a previously unrecognized JAZ repressor in Arabidopsis (JAZ13, encoded by At3g22275). JAZ13 is most closely related to JAZ8 and includes divergent EAR, TIFY/ZIM, and Jas motifs. Unlike JAZ8, however, JAZ13 contains a Ser-rich C-terminal tail that is a site for phosphorylation. Overexpression of JAZ13 resulted in reduced sensitivity to JA, attenuation of wound-induced expression of JA-response genes, and decreased resistance to insect herbivory. JAZ13 interacts with the bHLH transcription factor MYC2 and the co-repressor TOPLESS but, consistent with the absence of a TIFY motif, neither NINJA nor other JAZs. Analysis of single and higher-order T-DNA insertion jaz null mutants provided further evidence that JAZ13 is a repressor JA signaling. Our results demonstrate that proteins outside the TIFY family are functional JAZ repressors and further suggest that this expansion of the JAZ family allows fine-tuning of JA-mediated transcriptional responses.

Regulation of growth–defense balance by the JASMONATE ZIM‐DOMAIN (JAZ)‐MYC transcriptional module

Summary The plant hormone jasmonate (JA) promotes the degradation of JASMONATE ZIM‐DOMAIN (JAZ) proteins to relieve repression on diverse transcription factors (TFs) that execute JA responses. However, little is known about how combinatorial complexity among JAZ–TF interactions maintains control over myriad aspects of growth, development, reproduction, and immunity. We used loss‐of‐function mutations to define epistatic interactions within the core JA signaling pathway and to investigate the contribution of MYC TFs to JA responses in Arabidopsis thaliana. Constitutive JA signaling in a jaz quintuple mutant (jazQ) was largely eliminated by mutations that block JA synthesis or perception. Comparison of jazQ and a jazQ myc2 myc3 myc4 octuple mutant validated known functions of MYC2/3/4 in root growth, chlorophyll degradation, and susceptibility to the pathogen Pseudomonas syringae. We found that MYC TFs also control both the enhanced resistance of jazQ leaves to insect herbivory and restricted leaf growth of jazQ. Epistatic transcriptional profiles mirrored these phenotypes and further showed that triterpenoid biosynthetic and glucosinolate catabolic genes are up‐regulated in jazQ independently of MYC TFs. Our study highlights the utility of genetic epistasis to unravel the complexities of JAZ–TF interactions and demonstrates that MYC TFs exert master control over a JAZ‐repressible transcriptional hierarchy that governs growth–defense balance.

Molecular cloning of the tomato Hairless gene implicates actin dynamics in trichome-mediated defense and mechanical properties of stem tissue

Highlight This study implicates actin dynamics in glandular trichome development, cytosolic control of specialized metabolism, and mechanical properties of plant tissues.

Effects of hormonal priming on seed germination of pigeon pea under cadmium stress

In this work we investigated whether priming with auxin, cytokinin, gibberellin, abscisic acid and ethylene, alters the physiological responses of seeds of pigeon pea germinated under water and cadmium stress. Seeds treated with water or non-treated seeds were used as control. Although compared to non-treated seeds we found that the hormone treatments improve the germination of pigeon pea under cadmium stress, however, these treatments did not differ from water. However, we also observed a trend of tolerance to the effects of cadmium in the presence of ethylene, suggesting that the use of this hormone may be an efficient method to overcome seed germination under metal stress.

Molecular Mechanisms Affecting Cell Wall Properties and Leaf Architecture

Leaf architecture is determined by cell shape, size, and density. As plant cells are enclosed by a rigid cell wall, changes to leaf architecture have to occur through downstream genetic systems that induce alterations in (1) cell wall composition, (2) synthesis, assembly, and orientation of cytoskeletal elements and/or (3) the degree of cross-linkage between wall components in response to upstream developmental and environmental cues. This chapter reviews how leaf architecture is influenced by molecular mechanisms that modulate the above wall modification processes. Upstream signaling systems such as salicylic (SA), jasmonic (JA), and gibberellic (GA) acid have significant effects on leaf architecture. GA promotes and JA and SA suppress growth. Leaf architectural changes are brought about by these upstream systems in concert or in an interactive manner, and the associated downstream molecular systems that are involved in executing changes to cell wall properties will be discussed. Evidence will be provided to show that xyloglucan endotransglucosylase/hydrolase and pectin methyltransferase/pectin methylesterase/pectin methylesterase inhibitor systems are key downstream execution points of leaf architectural changes common to different upstream molecular systems. Optimization of leaf architecture maximizes light interception, gas exchange properties, and photosynthesis. In addition, plant growth has been shown to be more sensitive to leaf area than to area-based photosynthesis rate. Therefore, understanding genes and molecular mechanisms that affect cell wall properties and leaf architecture has broader implications in terms of crop improvement, and candidate genes that can be manipulated to optimize leaf architecture in order to maximize net carbon assimilation and plant growth will be proposed.