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Climate change is altering our environment, subjecting multiple agroecosystems worldwide to an increased frequency and intensity of abiotic stress conditions such as heat, drought, flooding, salinity, cold and/or their potential combinations. These stresses impact plant growth, yield and survival, causing losses of billions of dollars to agricultural productivity, and in extreme cases they lead to famine, migration and even wars. As the rate of change in our environment has dramatically accelerated in recent years, more research is urgently needed to discover and develop new ways and tools to increase the resilience of crops to different stress conditions. In this theme issue, new studies addressing the molecular, metabolic, and physiological responses of crops and other plants to abiotic stress challenges are discussed, as well as the potential to exploit these mechanisms in biotechnological applications aimed at preserving and/or increasing crop yield under our changing climate conditions. This article is part of the theme issue ‘Crops under stress: can we mitigate the impacts of climate change on agriculture and launch the ‘Resilience Revolution’?’ 

Climate change imposes abiotic stress on plants, significantly threatening global agriculture and food security. This indicates a need to apply our understanding of plant stress responses to improve crop resilience to these threats. Stress damages critical cellular components such as mitochondria, chloroplasts and the endoplasmic reticulum. Left unmitigated, abiotic stress can lead to cell death, which typically decreases overall plant health and productivity. Autophagy is a catabolic process that maintains cellular homeostasis by degrading and recycling damaged and dysfunctional cell components and organelles. Importantly, autophagy promotes plant tolerance to a wide range of environmental stresses, and manipulation of autophagy may lead to improved stress resilience in crops. Here, we discuss recent advances in our understanding of how autophagy affects abiotic stress resistance. We discuss the function of autophagy in different abiotic stresses (including nutrient stress, salt stress, drought, heat, cold, hypoxia, light stress and combined stresses) and provide insights from functional and genome-wide transcriptomic studies. We also evaluate the potential to enhance crop survival and productivity in suboptimal environmental conditions by activating autophagy, emphasizing the importance of targeted manipulation of key genes involved in the autophagy pathway. This article is part of the theme issue ‘Crops under stress: can we mitigate the impacts of climate change on agriculture and launch the ‘Resilience Revolution’?’. 

Abstract Weed control has relied on the use of organic and inorganic molecules that interfere with druggable targets, especially enzymes, for almost a century. This approach, although effective, has resulted in multiple cases of herbicide resistance. Furthermore, the rate of discovery of new druggable targets that are selective and with favorable environmental profiles has slowed down, highlighting the need for innovative control tools. The arrival of the biotechnology and genomics era gave hope to many that all sorts of new control tools would be developed. However, the reality is that most efforts have been limited to the development of transgenic crops with resistance to a few existing herbicides, which in fact is just another form of selectivity. Proteolysis‐targeting chimera (PROTAC) is a new technology developed to treat human diseases but that has potential for multiple applications in agriculture. This technology uses a small bait molecule linked to an E3 ligand. The 3‐dimensional structure of the bait favors physical interaction with a binding site in the target protein in a manner that allows E3 recruitment, ubiquitination and then proteasome‐mediated degradation. This system makes it possible to circumvent the need to find druggable targets because it can degrade structural proteins, transporters, transcription factors, and enzymes without the need to interact with the active site. PROTAC can help control herbicide‐resistant weeds as well as expand the number of biochemical targets that can be used for weed control. In the present article, we provide an overview of how PROTAC works and describe the possible applications for weed control as well as the challenges that this technology might face during development and implementation for field uses. © 2023 The Authors.Pest Management Sciencepublished by John Wiley & Sons Ltd on behalf of Society of Chemical Industry. 

Abstract Plant autophagy is a catabolic process where cellular components such as protein aggregates and dysfunctional organelles are degraded and recycled to maintain homeostasis and facilitate stress resilience. Autophagy relies on a double‐membrane vesicle called the autophagosome, which delivers cellular cargo to the vacuole for degradation. The Arabidopsis GFP‐ATG8 reporter line is a valuable tool widely used to visualize and quantify autophagosomes via microscopy and monitor autophagic degradation via immunoblotting. Consistent assessment of autophagic activity requires standardized protocols for sample preparation, imaging, and data analysis. Here, we present protocols for monitoring autophagy in Arabidopsis seedlings expressing GFP‐ATG8, including treatments to induce or inhibit autophagic flux, as well as imaging and image analysis procedures. These methods enable reliable evaluation of autophagic activity and can be adapted for diverse experimental conditions and genotypes. © 2025 The Author(s). Current Protocols published by Wiley Periodicals LLC. Basic Protocol 1: Growth of Arabidopsis seedlings Basic Protocol 2: Activation of autophagy in Arabidopsis seedlings by abiotic stresses Basic Protocol 3: Inhibition of vacuolar degradation by concanamycin A treatment Basic Protocol 4: Quantification of GFP‐ATG8‐labeled autophagosomes in Arabidopsis seedlings via microscopy Basic Protocol 5: Analysis of autophagic degradation of GFP‐ATG8 via immunoblotting 

Abstract In response to changing environmental conditions, plants activate cellular responses to enable them to adapt. One such response is autophagy, in which cellular components, for example proteins and organelles, are delivered to the vacuole for degradation. Autophagy is activated by a wide range of conditions, and the regulatory pathways controlling this activation are now being elucidated. However, key aspects of how these factors may function together to properly modulate autophagy in response to specific internal or external signals are yet to be discovered. In this review we discuss mechanisms for regulation of autophagy in response to environmental stress and disruptions in cell homeostasis. These pathways include post-translational modification of proteins required for autophagy activation and progression, control of protein stability of the autophagy machinery, and transcriptional regulation, resulting in changes in transcription of genes involved in autophagy. In particular, we highlight potential connections between the roles of key regulators and explore gaps in research, the filling of which can further our understanding of the autophagy regulatory network in plants. 

Abstract Eukaryotic cells have evolved membrane-bound organelles, including the endoplasmic reticulum (ER), Golgi, mitochondria, peroxisomes, chloroplasts (in plants and green algae) and lysosomes/vacuoles, for specialized functions. Organelle quality control and their proper interactions are crucial both for normal cell homeostasis and function and for environmental adaption. Dynamic turnover of organelles is tightly controlled, with autophagy playing an essential role. Autophagy is a programmed process for efficient clearing of unwanted or damaged macromolecules or organelles, transporting them to vacuoles for degradation and recycling and thereby enhancing plant environmental plasticity. The specific autophagic engulfment of organelles requires activation of a selective autophagy pathway, recognition of the organelle by a receptor, and selective incorporation of the organelle into autophagosomes. While some of the autophagy machinery and mechanisms for autophagic removal of organelles is conserved across eukaryotes, plants have also developed unique mechanisms and machinery for these pathways. In this review, we discuss recent progress in understanding autophagy regulation in plants, with a focus on autophagic degradation of membrane-bound organelles. We also raise some important outstanding questions to be addressed in the future. 

Abstract Autophagy, as an intracellular degradation system, plays a critical role in plant immunity. However, the involvement of autophagy in the plant immune system and its function in plant nematode resistance are largely unknown. Here, we show that root-knot nematode (RKN;Meloidogyne incognita) infection induces autophagy in tomato (Solanum lycopersicum) and differentatgmutants exhibit high sensitivity to RKNs. The jasmonate (JA) signaling negative regulators JASMONATE-ASSOCIATED MYC2-LIKE 1 (JAM1), JAM2 and JAM3 interact with ATG8s via an ATG8-interacting motif (AIM), and JAM1 is degraded by autophagy during RKN infection. JAM1 impairs the formation of a transcriptional activation complex between ETHYLENE RESPONSE FACTOR 1 (ERF1) and MEDIATOR 25 (MED25) and interferes with transcriptional regulation of JA-mediated defense-related genes by ERF1. Furthermore, ERF1 acts in a positive feedback loop and regulates autophagy activity by transcriptionally activatingATGexpression in response to RKN infection. Therefore, autophagy promotes JA-mediated defense against RKNs via forming a positive feedback circuit in the degradation of JAMs and transcriptional activation by ERF1. 

IntroductionVPS45 belongs to the Sec1/Munc18 family of proteins, which interact with and regulate Qa-SNARE function during membrane fusion. We have shown previously thatArabidopsis thalianaVPS45 interacts with the SYP61/SYP41/VTI12 SNARE complex, which locates on thetrans-Golgi network (TGN). It is required for SYP41 stability, and it functions in cargo trafficking to the vacuole and in cell expansion. It is also required for correct auxin distribution during gravitropism and lateral root growth. ResultsAsvps45knockout mutation is lethal in Arabidopsis, we identified a mutant,vps45-3, with a point mutation in theVPS45gene causing a serine 284-to-phenylalanine substitution. The VPS45-3 protein is stable and maintains interaction with SYP61 and SYP41. However,vps45-3plants display severe growth defects with significantly reduced organ and cell size, similar tovps45RNAi transgenic lines that have reduced VPS45 protein levels. Root hair and pollen tube elongation, both processes of tip growth, are highly compromised invps45-3. Mutant root hairs are shorter and thicker than those of wild-type plants, and are wavy. These root hairs have vacuolar defects, containing many small vacuoles, compared with WT root hairs with a single large vacuole occupying much of the cell volume. Pollen tubes were also significantly shorter invps45-3compared to WT. DiscussionWe thus show that VPS45 is essential for proper tip growth and propose that the observed vacuolar defects lead to loss of the turgor pressure needed for tip growth.