VOZ-dependent priming of salicylic acid-dependent defense against Rhizopus stolonifer by β-aminobutyric acid requires the TCP protein TCP2 in peach fruit.

Vascular plant one-zinc finger (VOZ) transcription factors (TFs) play crucial roles in plant immunity. Nevertheless, how VOZs modulate defense signaling in response to elicitor-induced resistance is not fully understood. Here, the defense elicitor β-aminobutyric acid (BABA) resulted in the visible suppression of Rhizopus rot disease of peach fruit caused by Rhizopus stolonifer.

β-aminobutyric acid-induced resistance in postharvest peach fruit involves interaction between the MAPK cascade and SNARE13 protein in salicylic acid-dependent pathway.

The inducer β-aminobutyric acid (BABA) is capable of immune response in various plants. However, the specific mitogen-activated protein kinase (MAPK) cascade involved in BABA-induced resistance (BABA-IR) has not yet been elucidated. Here, peach fruits treated with the BABA exhibited a pattern-triggered immunity (PTI) defense against Rhizopus stolonifer, accompanied by the generation of reactive oxygen species (ROS) and activation of MAPK cascade.

MADS2 regulates priming defence in postharvest peach through combined salicylic acid and abscisic acid signaling.

MADS-box genes play well-documented roles in plant development, but relatively little is known regarding their involvement in defence responses. In this study, pre-treatment of peach (Prunus persica) fruit with β-aminobutyric acid (BABA) activated resistance against Rhizopus stolonifer, leading to a significant delay in the symptomatic appearance of disease. This was associated with an integrated defence response that included a H2O2 burst, ABA accumulation, and callose deposition.

Corrigendum: Heat Shock Protein HSP24 Is Involved in the BABA-Induced Resistance to Fungal Pathogen in Postharvest Grapes Underlying an NPR1-Dependent Manner.

[This corrects the article DOI: 10.3389/fpls.2021.

Activation of the BABA-induced priming defence through redox homeostasis and the modules of TGA1 and MAPKK5 in postharvest peach fruit.

The priming of defence responses in pathogen-challenged model plants undergoes a preparation phase and an expression phase for defence function. However, the priming response in postharvest fruits has not been elucidated. Here, we found that 50 mM β-aminobutyric acid (BABA) treatment could induce two distinct pathways linked with TGA1-related systemic acquired resistance (SAR), resulting in the alleviation of Rhizopus rot in postharvest peach fruit.

Alterations in Sucrose and Phenylpropanoid Metabolism Affected by BABA-Primed Defense in Postharvest Grapes and the Associated Transcriptional Mechanism.

Defense elicitors can induce fruit disease resistance to control postharvest decay but may incur quality impairment. Our present work aimed to investigate the resistance against induced by the elicitor β-aminobutyric acid (BABA) and to elucidate the specific transcriptional mechanism implicated in defense-related metabolic regulations. The functional dissection results demonstrated that, after inoculation with the fungal necrotroph , a suite of critical genes encoding enzymes related to the sucrose metabolism and phenylpropanoid pathway in priming defense in grapes were transcriptionally induced by treatment with 10 mM BABA.

Heat Shock Protein HSP24 Is Involved in the BABA-Induced Resistance to Fungal Pathogen in Postharvest Grapes Underlying an NPR1-Dependent Manner.

Although heat shock proteins (HSPs), a family of ubiquitous molecular chaperones, are well characterized in heat stress-related responses, their function in plant defense remains largely unclear. Here, we report the role of , a class B HSP from , in β-aminobutyric acid (BABA)-induced priming defense against the necrotrophic fungus in grapes. Grapes treated with 10 mmol L BABA exhibited transiently increased transcript levels of and several SA-inducible genes, including , , and .

Dual function of VvWRKY18 transcription factor in the β-aminobutyric acid-activated priming defense in grapes.

Induction of phytoalexin production after invading pathogens is recognized as an essential aspect of the plant-induced resistance. The WRKY family includes plant-specific transcriptional factors associated with plant defense responses, but the comprehensive mechanisms are poorly understood. Here, we attempted to elaborate the regulatory function of VvWRKY18 from the group IIa of WRKY transcription factor (TF) from Vitis vinifera, in the regulation of β-aminobutyric acid (BABA)-activated stilbene phytoalexins biosynthesis and PATHOGENESIS-RELATED (PR) genes expressions in grapes.

β-aminobutyric acid induces priming defence against Botrytis cinerea in grapefruit by reducing intercellular redox status that modifies posttranslation of VvNPR1 and its interaction with VvTGA1.

Either NPR1 or TGA1 serve as master redox-sensitive transcriptional regulators for the transcription of PR genes in plants. The redox modification of the two co-activators involved in BABA-induced priming resistance against Botrytis cinerea in grapes was examined in this study. The results showed that 10 mmol L BABA could effectively trigger a priming defense in grapes as manifested by augmented expression levels of PR genes upon inoculation with B.