Salicylic acid activates poplar defense against the biotrophic rust fungusMelampsora larici‐populinavia increased biosynthesis of catechin and proanthocyanidins

Abstract

Poplar trees synthesize flavan-3-ols (catechin and proanthocyanidins) as a defense against foliar rust fungi, but the regulation of this defense response is poorly understood. Here, we investigated the role of hormones in regulating flavan-3-ol accumulation in poplar during rust infection. We profiled levels of defense hormones, signaling genes, and flavan-3-ol metabolites in black poplar leaves at different stages of rust infection. Hormone levels were manipulated by external sprays, genetic engineering, and drought to reveal their role in rust fungal defenses. Levels of salicylic acid (SA), jasmonic acid, and abscisic acid increased in rust-infected leaves and activated downstream signaling, with SA levels correlating closely with those of flavan-3-ols. Pretreatment with the SA analog benzothiadiazole increased flavan-3-ol accumulation by activating the MYB-bHLH-WD40 complex and reduced rust proliferation. Furthermore, transgenic poplar lines overproducing SA exhibited higher amounts of flavan-3-ols constitutively via the same transcriptional activation mechanism. These findings suggest a strong association among SA, flavan-3-ol biosynthesis, and rust resistance in poplars. Abscisic acid also promoted poplar defense against rust infection, but likely through stomatal immunity independent of flavan-3-ols. Jasmonic acid did not confer any apparent defense responses to the fungal pathogen. We conclude that SA activates flavan-3-ol biosynthesis in poplar against rust infection.

Strigolactones enhance root‐knot nematode (Meloidogyne graminicola) infection in rice by antagonizing the jasmonate pathway

“…The flow rate and the elution profile were similar to the method described by Ullah et al . (). The parent ion and corresponding fragments of SA and the jasmonates were analyzed by multiple reaction monitoring as described by Vadassery et al .…”

“…Hormones were separated on a Zorbax Eclipse XDB-C18 column (1.8 lm, 50 mm 9 4.6 mm; Agilent) at 25°C, with two mobile phases consisting of 0.05% formic acid in water and acetonitrile. The flow rate and the elution profile were similar to the method described by Ullah et al (2019). The parent ion and corresponding fragments of SA and the jasmonates were analyzed by multiple reaction monitoring as described by Vadassery et al (2012).…”

Metabolic and physiological analyses reveal that Populus cathayana males adopt an energy-saving strategy to cope with phosphorus deficiency

“…Therefore, it is worth being explored how sex-and tissue-specific JA changes caused by Pi deficiency may enhance tolerance against biotic or abiotic stresses in poplars. Metabolically, the sexually different SA and JA responses can be attributed to varying benzoic acid and phytodienoic acid contents in males and females, as these two organic acids are intermediates of the synthesis of SA and JA (Vlot et al 2009, Ullah et al 2019).…”

Hybridization disrupts growth-defense strategies and reveals trade-offs masked in unadmixed populations of a perennial plant

“…At the molecular level, the plant growth-defense trade-off is regulated by cellular signaling and hormonal regulation to direct metabolic activity away from growth and towards defense, or vice versa (Tian et al, 2003; Wang, 2012; Chandran et al, 2014). Host plant species may evolve a variety of costly defenses to combat disease, including the evolution of structural phenotypes to reduce exposure to pathogens (Gonzales-Vigil et al, 2017), immune systems to detect pathogens (Dangl and Jones, 2001) in order to initiate appropriate responses (Cai et al, 2018), and resistance via constitutive or inducible synthesis of defensive compounds (Bailey et al, 2005; Ullah et al, 2018). Hosts may also avoid disease by migrating out of environments where a pathogen spatially or temporally occurs (Altizer et al, 2011), by colonizing new environments where the pathogen is absent (Bruns et al, 2018), or by evolving life history strategies that avoid or compensate for pathogen exposure (Stearns, 1989).…”