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Biology subjects

Leibman-Markus, M.

Publications and source records attributed to Leibman-Markus, M..

4 recordsLinked to original sources

Immunity priming uncouples the growth-defense tradeoff in tomato

Plants have developed an array of mechanisms to protect themselves against pathogen invasion. The deployment of defense mechanisms is imperative for plant survival, but can come at the expense of plant growth, leading to the "growth- defense trade-off" phenomenon. Following pathogen exposure, plants can develop resistance to further attack. This is known as induced resistance, or priming. Here, we investigated the growth-defense trade-off, examining how defense priming via Systemic Acquired Resistance (SAR), or Induced Systemic Resistance (ISR), affects tomato development and growth. We found that defense priming can promote, rather than inhibit, plant development, and that defense priming and growth tradeoffs can be uncoupled. Cytokinin response was activated during induced resistance, and found to be required for the observed growth and disease resistance resulting from ISR activation. ISR was found to have a stronger effect on plant development than SAR. Our results suggest that growth promotion and induced resistance can be co-dependent, and that in certain cases, defense priming can drive developmental processes and promote plant yield. Summary statementGrowth-defense tradeoffs in plants result in loss of yield. Here, we demonstrate that immunity priming in different pathways uncouples this tradeoff and allows for disease resistant plants with robust growth.

plant biology↗

TOR mediates cytokinin-driven development and defense cues

Plants constantly perceive and process environmental signals and balance between the energetic demands of growth and defense. Growth arrest upon pathogen attack was previously suggested to result from a redirection of the plants metabolic resources towards the activation of plant defense. The energy sensor Target of Rapamycin (TOR) kinase is a conserved master coordinator of growth and development in all eukaryotes. Although TOR is positioned at the interface between development and defense, little is known about the mechanisms in which TOR may potentially regulate the relationship between these two modalities. The plant hormones cytokinin (CK) and gibberellin (GA) execute various aspects of plant development and defense. The ratio between CK and GA was reported to determine the outcome of developmental programs. Here, investigating the interplay between TOR-mediated development and TOR-mediated defense in tomato, we found that TOR silencing resulted in rescue of several different aberrant developmental phenotypes, demonstrating that TOR is required for the execution of developmental cues. In parallel, TOR inhibition enhanced immunity in genotypes with a low CK/GA ratio but not in genotypes with a high CK/GA ratio. TOR-inhibition mediated disease resistance was found to depend on developmental status, and was abolished in strongly morphogenetic leaves, while being strongest in mature, differentiated leaves. CK repressed TOR activity, suggesting that CK-mediated immunity may rely on TOR downregulation. At the same time, TOR activity was promoted by GA, and TOR silencing reduced GA sensitivity, indicating that GA signaling requires normal TOR activity. Our results demonstrate that TOR likely acts in concert with CK and GA signaling, executing signaling cues in both defense and development. Thus, differential regulation of TOR or TOR-mediated processes could regulate the required outcome of development-defense prioritization.

plant biology↗

Cytokinin- microbiome interactions regulate developmental functions

The interaction of plants with the complex microbial networks that inhabit them is important for plant health. While the reliance of plants on their microbial inhabitants for defense against invading pathogens is well documented, the acquisition of data concerning the relationships between plant developmental stage or aging, and microbiome assembly, is still underway. In this work, we observed developmental-age dependent changes in the phyllopshere microbiome of tomato. The plant hormone cytokinin (CK) regulates various plant growth and developmental processes. Here, we show that age-related shifts in microbiome content vary based on content of, or sensitivity to, CK. We observed a developmental age associated decline in microbial richness and diversity, accompanied by a decline in the presence of growth promoting and resistance inducing bacilli in the phyllosphere. This decline was absent from CK-rich or CK-hypersensitive genotypes. Bacillus isolates we obtained from CK rich genotypes were found to re-program the transcriptome to support morphogenesis and alter the leaf developmental program when applied to seedlings, and enhance yield and agricultural productivity when applied to mature plants. Our results support the notion that CK-dependent effects on microbiome content support developmental functions, suggesting that these are mediated by CK in part via the bacterial community.

plant biology↗

Cytokinin response induces immunity and fungal pathogen resistance in tomato by modulating cellular trafficking of PRRs

Plant immunity is often defined by the "immunity hormones": salicylic acid (SA), jasmonic acid (JA), and ethylene (ET). These hormones are well known for differentially regulating defense responses against pathogens. In recent years, the involvement of other plant growth hormones such as auxin, gibberellic acid, abscisic acid, and cytokinins (CKs) in biotic stresses has been recognized. Previous reports have indicated that endogenous and exogenous CK treatment can result in pathogen resistance. We show here that CK induces systemic tomato immunity, modulating cellular trafficking of the PRR LeEIX2 and promoting biotrophic and necrotrophic pathogen resistance in an SA and ET dependent mechanism. CK perception within the host underlies its protective effect. Our results support the notion that CK acts as a priming agent, promoting pathogen resistance by inducing immunity in the host.

plant biology↗