Insights Into the Mechanisms Implicated in Pinus pinaster Resistance to Pinewood Nematode

Pine wilt disease (PWD), caused by the plant–parasitic nematode Bursaphelenchus xylophilus, has become a severe environmental problem in the Iberian Peninsula with devastating effects in Pinus pinaster forests. Despite the high levels of this species' susceptibility, previous studies reported heritable resistance in P. pinaster trees. Understanding the basis of this resistance can be of extreme relevance for future programs aiming at reducing the disease impact on P. pinaster forests. In this study, we highlighted the mechanisms possibly involved in P. pinaster resistance to PWD, by comparing the transcriptional changes between resistant and susceptible plants after infection. Our analysis revealed a higher number of differentially expressed genes (DEGs) in resistant plants (1,916) when compared with susceptible plants (1,226). Resistance to PWN is mediated by the induction of the jasmonic acid (JA) defense pathway, secondary metabolism pathways, lignin synthesis, oxidative stress response genes, and resistance genes. Quantification of the acetyl bromide-soluble lignin confirmed a significant increase of cell wall lignification of stem tissues around the inoculation zone in resistant plants. In addition to less lignified cell walls, susceptibility to the pine wood nematode seems associated with the activation of the salicylic acid (SA) defense pathway at 72 hpi, as revealed by the higher SA levels in the tissues of susceptible plants. Cell wall reinforcement and hormone signaling mechanisms seem therefore essential for a resistance response.

Fast Spectrophotometric Method as Alternative for CuO Oxidation to Assess Lignin in Soils with Different Tree Cover

Given the ongoing climate change, estimating the amount of less degradable plant compounds that can be stored in the soil, such as lignin, is a topic of primary importance. There are few methods applicable to soils for the determination of lignin, such as the copper oxide (CuO) oxidation method (CuOL). Acetyl bromide spectrophotometric lignin (ABSL) could be a valid alternative providing information that is less detailed compared to CuOL, but it offers data on the bulk amount of lignin and may offer a valid, fast, and cheap alternative to the CuO method. The aim of this work was to compare ABSL with the CuO method on several soils receiving plant residues from different trees. Mineral soil samples from 0 to 10 cm depth were obtained from a former agricultural site in northern Italy (Brusciana, Tuscany), where different tree plantations were established 22 years ago. The plantations were white poplar and common walnut, which were also intercropped with other species such as hazelnut, Italian alder, and autumn olive. Soil samples under these plantations were also compared to soil under an adjacent agricultural field. In general, the amount of lignin in the afforested stands was approximately double than in the agricultural field as determined by either method. The two methods returned a largely different scale of values due to their different mechanisms of action. The acid-to-aldehyde ratio of syringyl structural units highlights that forest plantation provides a plant input material that is more slowly oxidatively degraded compared to arable soil. A linear mixed model proved that ABSL performed well in relation to CuOL, especially when considering the random variation in the model given by the plantation field design. In conclusion, ABSL can be considered a valid proxy of soil C pool derived from structural plant component, although further analyses are needed.

Transcriptomic study of pedicels from GA3-treated table grape genotypes with different susceptibility to berry drop reveals responses elicited in cell wall yield, primary growth and phenylpropanoids synthesis.

Background Gibberellins (GA3) are the most sprayed growth regulator for table grape production worldwide, increasing berry size of seedless varieties through pericarp cell expansion. However, these treatments also exacerbate berry drop, which has a detrimental effect on the postharvest quality of commercialized clusters. Several studies have suggested that pedicel stiffening caused by GA3 would have a role in this disorder. Nevertheless, transcriptional and phenotypic information regarding pedicel responses to GA3 is minimal.Results Characterization of responses to GA3 treatments using the lines L23 and Thompson Seedless showed that the former was up to six times more susceptible to berry drop than the latter. GA3 also increased the diameter and dry matter percentage of the pedicel on both genotypes. Induction of lignin biosynthesis-related genes by GA3 has been reported, so the quantity of this polymer was measured. The acetyl bromide method detected a decreased concentration of lignin seven days after GA3 treatment, due to a higher cell wall yield of the isolated fractions of GA3-treated pedicel samples which caused a dilution effect. Thus, an initial enrichment of primary cell wall components in response to GA3 was suggested, particularly in the L23 background. A transcriptomic profiling was performed to identify which genes were associated with these phenotypic changes. This analysis identified 1,281 and 1,787 genes differentially upregulated by GA3 in L23 and cv. Thompson Seedless, respectively. Concomitantly, 1,202 and 1,317 downregulated genes were detected in L23 and cv. Thompson Seedless (FDR≤0.05). Gene ontology analysis of upregulated genes showed enrichment in pathways including phenylpropanoids, cell wall metabolism, xylem development, photosynthesis and the cell cycle at seven days post GA3 application. Twelve genes were characterized by qPCR and striking differences were observed between genotypes, mainly in genes related to cell wall synthesis.Conclusions High levels of berry drop are related to an early strong response of primary cell wall synthesis in the pedicel promoted by GA3 treatment. Genetic backgrounds can produce similar phenotypic responses to GA3, although there is considerable variation in the regulation of genes in terms of which are expressed, and the extent of transcript levels achieved within the same time frame.

Lignin Content and Resistance to Sclerotinia minor in Peanut

ABSTRACT Lignin has been shown to be an important component for plant defense in several pathosystems, but the relationship between peanut stem lignin content and resistance in the field to Sclerotinia blight has not been investigated. Stem lignin was quantified from twenty runner, six virginia, and ten spanish genotypes grown in the greenhouse using the acetyl bromide method. Significant differences in lignin content were found within the runner and spanish entries, but not among the virginia genotypes. Disease data collected in the field over two to three years were used to test correlations between lignin content and Sclerotinia blight resistance for a subset of the runner and virginia entries. No significant correlations were found. Within the runner entries, the highest and lowest stem lignin content was found in entries with the most disease resistance. These results indicate that preformed stem lignin content is not a reliable predictor for resistance to Sclerotinia blight in peanut. In addition, commercial peanut cultivars appear to vary considerably in lignin content, and the genotypes with lower levels of stem lignin may be useful to producers who can use peanut haulm for animal feed. Southwest Runner, a cultivar with high resistance to Sclerotinia blight, had the lowest stem lignin content of the 36 peanut lines tested.

Hydroxycinnamic Acid Degradation, a Broadly Conserved Trait, Protects Ralstonia solanacearum from Chemical Plant Defenses and Contributes to Root Colonization and Virulence

Plants produce hydroxycinnamic acid (HCA) defense compounds to combat pathogens, such as the bacterium Ralstonia solanacearum. We showed that an HCA degradation pathway is genetically and functionally conserved across diverse R. solanacearum strains. Further, a feruloyl-CoA synthetase (Δfcs) mutant that cannot degrade HCA was less virulent on tomato plants. To understand the role of HCA degradation in bacterial wilt disease, we tested the following hypotheses: HCA degradation helps the pathogen i) grow, as a carbon source; ii) spread, by reducing HCA-derived physical barriers; and iii) survive plant antimicrobial compounds. Although HCA degradation enabled R. solanacearum growth on HCA in vitro, HCA degradation was dispensable for growth in xylem sap and root exudate, suggesting that HCA are not significant carbon sources in planta. Acetyl-bromide quantification of lignin demonstrated that R. solanacearum infections did not affect the gross quantity or distribution of stem lignin. However, the Δfcs mutant was significantly more susceptible to inhibition by two HCA, namely, caffeate and p-coumarate. Finally, plant colonization assays suggested that HCA degradation facilitates early stages of infection and root colonization. Together, these results indicated that ability to degrade HCA contributes to bacterial wilt virulence by facilitating root entry and by protecting the pathogen from HCA toxicity.