![]() Numerous studies have reported that hormones, such as salicylic acid (SA), jasmonic acid (JA), and ethylene (ET), mount plant defense responses to invading herbivores. Therefore, it is a pivotal target for compromising plant defense by adjusting the hormone level, timing, and composition. Īlthough the defensive strategies vary substantially across different plant species, the defense pathways regulated by hormones are somewhat conserved. Additionally, plants also own an efficient basal defense system, and this process relies on the perception of wounding signals caused by aphid stylets during the penetration for feeding, and/or and transmission of salivary secretion-derived chemical cues into the host, thereby eliciting the generation of signaling molecules that invoke a common stress response. The race-specific resistant process involves gene-for-gene interaction, in which an effector protein derived from the insect can be recognized by its corresponding host resistance (R) protein, and further activates specific defense pathways to hamper pest invasion. Plant defense responses to aphids are modulated by both race-specific resistance and plant basal defense. Nevertheless, punctuation of sieve elements by aphid stylets and salivary secretions still provoke active defense responses in host plants. During aphid-host plant interactions, aphids can minimize mechanical wounding and avert triggering intracellular and extracellular defenses by the secretion of gelling and watery saliva. Plants have developed constitutive and induced defense tactics, such as physical obstacles (e.g., cuticles, cell walls, and trichomes), and chemical defense (e.g., secondary metabolites) to prevent the infestation of phloem sap feeders. In higher plants, a set of sophisticated strategies has been employed to withstand the attacks from a variety of herbivorous insects during long-term coevolution. Collectively, our findings indicate that the Arabidopsis MYB102 increases host susceptibility to GPA through the ET-dependent signaling pathways. Conversely, overexpression of MYB102 failed to increase aphid susceptibility in both the ET-insensitive mutants and plants treated with inhibitors of ET signaling pathways, demonstrating that the ET was critical for promoting aphid performance conferred by overexpression of MYB102. Overexpression of MYB102 in Arabidopsis obviously repressed aphid-induced callose deposition. In agreement with a negative regulatory role for ET in aphid defense responses, the MYB102-overexpressing lines were more susceptible to GPA than wild-type (WT) plants. Furthermore, dominant suppression of MYB102 inhibited aphid-induced increase of ET levels in Arabidopsis. Enhanced ET levels led to reduced Arabidopsis resistance to GPA. The results of RNA-Sequencing revealed that overexpression of MYB102 in Arabidopsis promoted ET biosynthesis by upregulation of some 1-aminocyclopropane-1-carboxylate synthase (ACS) genes, which are rate-limiting enzymes of the ET-synthetic pathway. Arabidopsis MYB102 was primarily expressed in vascular tissues, and its transcription was remarkably induced by green peach aphids (GPA Myzus persicae). Here, we investigated the function of MYB102 in the response of Arabidopsis to aphid infestation. However, it remains unclear whether Arabidopsis MYB102 takes part in the defense response of plants to aphids. Arabidopsis MYB102 has previously been shown to be induced by wound signaling and regulate defense response against chewing insects. Recent studies have indicated that some MYB transcription factors regulate the phloem-based defense against aphid infestation by modulating ethylene (ET) signaling. Induction of ethylene biosynthesis by aphids increases the susceptibility of several plant species to aphids.
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