Abstract WRKY transcription factors and jasmonic acid (JA) signaling are essential for plant responses to stress, but their roles in strawberry resistance to Botrytis cinerea remain unclear. Here, we investigated the function of FaWRKY7 in strawberry fruit and transgenic Arabidopsis thaliana. FaWRKY7 expression was significantly induced at 72 h after B. cinerea inoculation. Transient overexpression of FaWRKY7 enhanced strawberry fruit resistance to B. cinerea, whereas silencing increased susceptibility. Similarly, FaWRKY7-overexpressing Arabidopsis plants showed enhanced resistance to B. cinerea and greater responsiveness to exogenous methyl jasmonate (MeJA), although basal levels of free JA, JA-Ile, and OPDA were not detectably altered in non-inoculated samples. Pharmacological assays further showed that FaWRKY7-mediated resistance was maintained under MeJA treatment and only partially reduced by Jarin-1, an inhibitor of JA-Ile formation, indicating that this effect is only partially dependent on JA-Ile formation. Mechanistically, DAP-seq, yeast one-hybrid, EMSA, and dual-luciferase assays showed that FaWRKY7 directly binds to the promoters of FaJAZ4 and FaJAZ8 and represses their transcription. These findings indicate that FaWRKY7 enhances resistance to B. cinerea, at least in part by directly repressing FaJAZ4 and FaJAZ8 and thereby modulating jasmonate signaling responses.
Abstract Plant-herbivore interactions are shaped not only by plant defensive responses but also by herbivore perception of host-associated chemical cues. However, how tea plants coordinate chemical defenses and how Helopeltis theivora responds behaviorally to induced plant signals remain poorly understood. Here, we combined transcriptomic, metabolomic, behavioral, and electrophysiological approaches to dissect the molecular mechanisms underlying tea defense activation and herbivore behavioral adaptation. Following H. theivora infestation, JA signaling and its bioactive derivatives were rapidly induced. Meanwhile, phenylalanine accumulation and auxin metabolic remodeling increased progressively with infestation pressure. Integrated transcriptomic and metabolomic analyses revealed coordinated activation of the phenylpropanoid-flavonoid pathway as a central metabolic defense module. Pinobanksin-3-acetate accumulated substantially and was identified as a potential chemical component contributing to tea resistance. In parallel, feeding-induced (E)-β-ocimene emission increased significantly and elicited dose-dependent behavioral avoidance in adult male H. theivora, suggesting that this volatile may function as an olfactory cue for assessing host defensive status. Together, our findings reveal a complex ecological consequence of herbivore-induced defense: tea plants enhance metabolic resistance while simultaneously releasing volatile signals that may influence herbivore host-selection behavior. These insights provide potential chemical targets for developing sustainable pest management strategies through manipulation of plant defense pathways and insect behavioral responses.
Abstract Climate change exposes plants to recurrent and interacting stresses, yet the extent to which these effects persist across generations, and the mechanisms involved, remain unclear. Here, we compared Arabidopsis thaliana wild type (WT, Col-0) plants with gsnor1-3 (hereafter, gsnor-ko), a mutant deficient in S-nitrosoglutathione reductase (GSNOR), an enzyme involved in nitric oxide homeostasis. Plants were propagated for three successive generations (G1-G3) under control, drought, elevated CO2, O3, heat (warm temperature), and combined treatment scenarios, followed by two recovery generations under control conditions (G4-G5). We quantified rosette growth, photosynthetic traits, seed production, and transcriptome dynamics by RNA-seq. Across environments, gsnor-ko exhibited reduced vegetative growth and reproductive output compared with WT. Transcriptomic responses were strongly scenario- and generation-dependent, with the largest differential expression shifts observed under heat and combined-treatment (combination) conditions. Compared with WT, gsnor-ko showed greater transcriptome similarity across generations and among genes differentially expressed in response to the same treatment. Functional enrichment and candidate-gene analyses identified pathways/components linked to DNA methylation, heterochromatin maintenance, histone ubiquitination, m6A RNA regulation, and methyl-donor metabolism. Together, these findings are consistent with a model in which GSNOR activity contributes to transcriptomic recovery after repeated climate stress, whereas GSNOR deficiency is associated with recurrent or reconfigured stress-associated transcriptional states at G1, G3, and G5, suggesting epigenetically associated regulatory reconfiguration.
Abstract The work proposed a correlative inhibition (CI) model based on positive feedback (PF) between sugars (Sug) and cytokinis (CKs) - CK activates Sug uploading to sink organs, and Sug increases CK content and activates CK signalling. This creates an unstable PF system capable of triggering the development of dominant and suppressed shoots on the same plant. The predictions of the Sug-CK model were tested on two-branched pea seedlings. Sug deficiency (removal of part of the cotyledons) and CK deficiency (treatment with an inhibitor of CK synthesis) in accordance with the model increased the occurrence of unequal-branched plants. Surprisingly, auxin was found to be inactive in the regulation of CI. In the apical buds of lateral shoots, a Sug deficiency reduced the CK signal, as measured by the expression of PsRR5 gene, whilst inhibition of CK synthesis reduced Sug accumulation, thereby confirming the presence of PF between CK and Sug. A deficiency of Sug enhanced the effect of a CK deficiency in reducing CK status, explaining the synergistic effect of both deficiencies on CI. A deficiency of strigolactones (SL) in the rms5 and rms1 mutants and SL insensitivity in the rms4 mutant completely abolished the effects of CK and Sug deficiencies on CI. It was demonstrated on the rms5 mutant that a CK deficiency did not affect Sug levels thus explaining the insensitivity to CK-Sug deficiencies in SL mutants. The BRANCHED1 (BRC1) gene is an important regulator of plant branching, and its absence in the brc1 mutant resulted in a lack of response to Sug deficiency with regard to both CI and CK status. It has thus been shown that SL signalling and the BRC1 gene are involved in the Sug-CK interaction, thereby playing a role in the regulation of CI.
Abstract Phosphorus (P) is an essential plant nutrient with low bioavailability in soils, and its uptake and that of nitrogen (N) are crucial for optimal growth. Here, diverse maize genotypes with distinct breeding histories, including doubled haploids from landraces, were grown under two P levels. The genotypes showed substantial variation in internal P concentrations and in performance under low P. Several lines maintained adequate N regardless of P supply; however, two lines from the heterotic dent pool performed poorly under low P and exhibited N deficiency. Only these lines lacked a robust transcriptional phosphate starvation response (PSR) in roots. Although N-related gene expression varied among lines, it did not explain differences in N acquisition. Inositol pyrophosphates (PP-InsPs), potential key regulators of P status signalling, were similarly diminished in contrasting lines under P deficiency, suggesting that they may be required, but not sufficient for PSR responses in roots. Overall, the results reveal large genotypic variation in low-P responses, line-specific N–P interactions at the post-transcriptional level and a critical role of shoot-root communication, which are discussed in the context of differential responses to P availability.
