Yanping Jing

Salt stress represents one of the most critical abiotic constraints limiting global agricultural productivity by adversely affecting plant growth, metabolism, and yield. Soil salinization disrupts water uptake and nutrient homeostasis, leading to ionic toxicity, osmotic imbalance, and oxidative stress that collectively impair crop development. Cucumis melo, a major horticultural crop of significant economic value, exhibits high sensitivity to salinity. Recent advances have elucidated that melon adapts to salt stress through intricate physiological and molecular mechanisms involving osmotic adjustment, ion transport regulation, antioxidant defense, and transcriptional reprogramming. Several pivotal genes, such as CmNHX1, CmHKT1;1, CmCML13, CmAPX27, and CmRAV1, etc., have been identified to participate in multiple signaling pathways governing salt tolerance in melon. In this review, we comprehensively summarize the physiological effects of salt stress on melon growth, elucidating the key molecular mechanisms underlying salt tolerance, particularly those associated with ion homeostasis, antioxidant defense, and transcriptional regulation. The review further discusses current strategies and future perspectives for the genetic improvement of salt tolerance. Collectively, this review provides a theoretical framework and valuable reference for future research on the molecular basis of salt tolerance and breeding of salt-tolerant melon cultivars.

Soil degradation and pollution pose significant threats to global agricultural sustainability and food security. Conventional remediation methods are often constrained by low efficiency, high cost, and potential secondary pollution. Nanobiotechnology, an emerging interdisciplinary field, offers innovative solutions by integrating functional nanomaterials with plant–microbe interactions to advance soil remediation and sustainable agriculture. This review systematically elaborates on the mechanisms and applications of nanomaterials in soil remediation and enhanced plant stress resilience. For contaminant removal, nanomaterials such as nano-zero-valent iron (nZVI) and carbon nanotubes effectively immobilize or degrade heavy metals and organic pollutants through adsorption, catalysis, and other reactive mechanisms. In agriculture, nanofertilizers facilitate the regulated release of nutrients, thereby markedly enhancing nutrient use efficiency. Concurrently, certain nanoparticles mitigate a range of abiotic stresses—such as drought, salinity, and heavy metal toxicity—through the regulation of phytohormone balance, augmentation of photosynthetic performance, and reinforcement of antioxidant defenses. However, concerns regarding the environmental behavior, ecotoxicity, and long-term safety of nanomaterials remain. Future research should prioritize the development of smart, responsive nanosystems, elucidate the complex interactions among nanomaterials, plants, and microbes, and establish comprehensive life-cycle assessment and standardized risk evaluation frameworks. These efforts are essential to ensuring the safe and scalable application of nanobiotechnology in environmental remediation and green agriculture.

Background and Aims: Plant elicitor peptides (Peps), which originate from their precursor proteins known as PROPEPs, play essential roles as signaling molecules that modulate both plant defense responses and developmental processes. Methods: In this study, we investigated the role of PROPEP2 and its derived peptide Pep2, in regulating root hair development in Arabidopsis thaliana. Root hairs at different growth stages along the primary root and in distinct zones of the root tip were analyzed. We further examined the relationship between Pep2 and auxin signaling in regulating root hair growth. Key results: Our findings indicate that loss of PROPEP2 function results in markedly decreased root hair number and elongation during the primary root development phase, whereas root hair formation during the embryonic root stage remains unaffected. Notably, exogenous Pep2 application rescued these defects and even induced root hair formation in non-hair-forming regions. We further demonstrated that Pep2 enhances root hair growth by stimulating localized auxin production in the root tip region. The mutants defective in auxin production (yuc1 yuc4 and wei8 tar1 tar2) failed to respond to Pep2. Furthermore, we identified the receptor-like kinases FERONIA (FER) and [Ca2+]cyt-associated protein kinase 1 (CAP1) as critical components of the Pep2 signaling pathway, with mutations in these genes impairing root hair growth and rendering plants unresponsive to Pep2. Conclusions: These results uncover a previously uncharacterized interaction between Pep2 and auxin signaling components in the regulation of root hair development, offering additional insights into the molecular control of root morphology.

Plant Elicitor Peptides (Peps) induce plant immune responses and inhibit root growth through their receptors PEPR1 and PEPR2, two receptor-like kinases. In our study, we found a previously unknown function of Peps that enhance root hair growth in a PEPRs-independent manner. When we characterized the expression patterns of PROPEP genes, we found several gene promoters of PROPEP gene family were particularly active in root hairs. Furthermore, we observed that PROPEP2 is vital for root hair development, as disruption of PROPEP2 gene led to a significant reduction in root hair density and length. We also discovered that PROPEP2 regulates root hair formation via the modulation of CPC and GL2 expression, thereby influencing the cell-fate determination of root hairs. Additionally, calcium signaling appeared to be involved in PROPEP2/Pep2-induced root hair growth. These findings shed light on the function of Peps in root hair development.

In plants, the regulation of plasma membrane (PM) dynamics through endocytosis plays a crucial role in responding to external environmental cues and defending against pathogens. The Arabidopsis plant elicitor peptides (Peps), originating from precursor proteins called PROPEPs, have been implicated in various aspects of plant immunity. This study delves into the signaling pathway of Peps, particularly Pep1, and its effect on PM protein internalization. Using PIN2 and BRI1 as PM markers, we demonstrated that Pep1 stimulates the endocytosis of these PM-localized proteins through clathrin-mediated endocytosis (CME). CLC2 and CLC3, two light chains of clathrin, are vital for Pep1-induced PIN2-GFP and BRI1-GFP internalization.The internalized PIN2 and BRI1 are subsequently transported to the vacuole via the trans-Golgi network/early endosome (TGN/EE) and prevacuolar compartment (PVC) pathways. Intriguingly, salicylic acid (SA) negatively regulates the effect of Pep1 on PM endocytosis. This study sheds light on a previously unknown signaling pathway by which danger peptides like Pep1 influence PM dynamics, contributing to a deeper understanding of the function of plant elicitor peptide.

The remodeling of root architecture is regarded as a major development to improve the plant’s adaptivity to phosphate (Pi)-deficient conditions. The WRKY transcription factors family has been reported to regulate the Pi-deficiency-induced systemic responses by affecting Pi absorption or transportation. Whether these transcription factors act as a regulator to mediate the Pi-deficiency-induced remodeling of root architecture, a typical local response, is still unclear. Here, we identified an Arabidopsis transcription factor, WRKY33, that acted as a negative regulator to mediate the Pi-deficiency-induced remodeling of root architecture. The disruption of WRKY33 in wrky33-2 mutant increased the plant’s low Pi sensitivity by further inhibiting the primary root growth and promoting the formation of root hair. Furthermore, we revealed that WRKY33 negatively regulated the remodeling of root architecture by controlling the transcriptional expression of ALMT1 under Pi-deficient conditions, which further mediated the Fe³⁺ accumulation in root tips to inhibit the root growth. In conclusion, this study demonstrates a previously unrecognized signaling crosstalk between WRKY33 and the ALMT1-mediated malate transport system to regulate the Pi deficiency responses.

Plant elicitor peptides (Peps) are damage/danger-associated molecular patterns (DAMPs) that are derived from precursor proteins PROPEPs and perceived by a pair of leucine-rich repeat receptor-like kinases (LRR-RLKs), PEPR1 and PEPR2, to enhance innate immunity and to inhibit root growth in Arabidopsis thaliana. In this study, we show that Arabidopsis Pep1 inhibits the root growth by interfering with pH signaling, as acidic condition increased, but neutral and alkaline conditions decreased the Pep1 effect on inhibiting the root growth. The perception of Pep1 to PEPRs activated the plasma membrane-localized H+-ATPases (PM H+-ATPases) —the pump proton in plant cell—to extrude the protons into apoplast, and induced an overly acidic environment in apoplastic space, which further promoted the cell swelling in root apex and inhibited root growth. Furthermore, we revealed that pump proton AUTOINHIBITED H⁺-ATPase 2 (AHA2) physically interacted with PEPR2 and served downstream of the Pep1-PEPRs signaling pathway to regulate Pep1-induced protons extrusion and root growth inhibition. In conclusion, this study demonstrates a previously unrecognized signaling crosstalk between Pep1 and pH signaling to regulate root growth.

Plant elicitor peptides (Peps) are damage/danger-associated molecular patterns (DAMPs) that are perceived by a pair of receptor-like kinases, PEPR1 and PEPR2, to enhance innate immunity and induce the growth inhibition of root in Arabidopsis thaliana. In this study, we show that PEPR1 and PEPR2 function vitally in roots to regulate the root immune responses when treating the roots with bacterial pathogen Pst DC3000. PEPR2, rather than PEPR1, played a predominant role in the perception of Pep1 in the roots and further triggered a strong ROS accumulation—the substance acts as an antimicrobial agent or as a secondary messenger in plant cells. Consistently, seedlings mutating two major ROS-generating enzyme genes, respiratory burst oxidase homologs D and F (RBOHD and RBOHF), abolished the root ROS accumulation and impaired the growth inhibition of the roots induced by Pep1. Furthermore, we revealed that botrytis-induced kinase 1 (BIK1) physically interacted with PEPRs and RBOHD/F, respectively, and served downstream of the Pep1-PEPRs signaling pathway to regulate Pep1-induced ROS production and root growth inhibition. In conclusion, this study demonstrates a previously unrecognized signaling crosstalk between Pep1 and ROS signaling to regulate root immune response and root growth.

Plant elicitor peptides (Peps) are damage/danger-associated molecular patterns that are perceived by the receptor-like kinases, PEPR1 and PEPR2, to enhance innate immunity and to inhibit root growth in Arabidopsis (Arabidopsis thaliana). Here, we show that Arabidopsis Pep1 inhibits root growth in a PEPR2-dependent manner, which is accompanied by swelling epidermal and cortex cells and root hair formation in the transition zone (TZ). These Pep1-induced changes were mimicked by exogenous auxin application and were suppressed in the auxin perception mutants transport inhibitor response1 (tir1) and tir1 afb1 afb2. Pep1-induced auxin accumulation in the TZ region preceded cell expansion in roots. Because local auxin distribution depends on PIN-type auxin transporters, we examined Pep1-PEPR-induced root growth inhibition in several pin mutants and found that pin2 was highly sensitive but pin3 was less sensitive to Pep1. The pin2 pin3 double mutant was as sensitive to Pep1 treatment as wild-type plants. Pep1 reduced the abundance of PIN2 in the plasma membrane through activating endocytosis while increasing PIN3 expression in the TZ, leading to changes in local auxin distribution and inhibiting root growth. These results suggest that Pep-PEPR signaling undergoes crosstalk with auxin accumulation to control cell expansion and differentiation in roots during immune responses.