Crop loss due to soil salinization is an increasing threat to agriculture worldwide. This review provides an overview of cellular and physiological mechanisms in plant responses to salt. We place cellular responses in a time- and tissue-dependent context in order to link them to observed phases in growth rate that occur in response to stress. Recent advances in phenotyping can now functionally or genetically link cellular signaling responses, ion transport, water management, and gene expression to growth, development, and survival. Halophytes, which are naturally salt-tolerant plants, are highlighted as success stories to learn from. We emphasize that ( a) filling the major knowledge gaps in salt-induced signaling pathways, ( b) increasing the spatial and temporal resolution of our knowledge of salt stress responses, ( c) discovering and considering crop-specific responses, and ( d) including halophytes in our comparative studies are all essential in order to take our approaches to increasing crop yields in saline soils to the next level.
The current model for vesicular traffic to and from the plasma membrane is accepted, but the molecular requirements for this coordination are not well defined. We have identified the hot ABA-deficiency suppressor1 mutant, which has a stomatal function defect, as a clathrin heavy chain1 (CHC1) mutant allele and show that it has a decreased rate of endocytosis and growth defects that are shared with other chc1 mutant alleles. We used chc1 alleles and the related chc2 mutant as tools to investigate the effects that clathrin defects have on secretion pathways and plant growth. We show that secretion and endocytosis at the plasma membrane are sensitive to CHC1 and CHC2 function in seedling roots and that chc mutants have physiological defects in stomatal function and plant growth that have not been described previously. These findings suggest that clathrin supports specific functions in multiple cell types. Stomata movement and gas exchange are altered in chc mutants, indicating that clathrin is important for stomatal regulation. The aberrant function of chc mutant stomata is consistent with the growth phenotypes observed under different water and light conditions, which also are similar to those of the secretory SNARE mutant, syp121. The syp121 and chc mutants have impaired endocytosis and exocytosis compared with the wild type, indicating a link between SYP121-dependent secretion and clathrin-dependent endocytosis at the plasma membrane. Our findings provide evidence that clathrin and SYP121 functions are important for the coordination of endocytosis and exocytosis and have an impact on stomatal function, gas exchange, and vegetative growth in Arabidopsis (Arabidopsis thaliana).
Due to its detrimental effect on plant growth, salinity is an increasing worldwide problem for agriculture. To understand the molecular mechanisms activated in response to salt in Arabidopsis, we investigated the Catharanthus roseus Receptor like Kinase 1 Like family, containing sensors previously shown to be involved in sensing the structural integrity of the cell walls. We found that herk1the1-4 double mutants, lacking the function of HERKULES1 (HERK1) combined with a gain-of-function allele of THESEUS1 (THE1), strongly respond to salt application, resulting in an intense activation of stress responses, similarly to plants lacking FERONIA (FER) function. We report that salt triggers pectin methyl esterase (PME) activation and show its requirement for the activation of several salt-dependent responses. Because chemical inhibition of PMEs alleviates these salt-induced responses, we hypothesize a model where salt directly leads to cell wall modifications through the activation of PMEs. Responses to salt partly require the functionality of FER alone or the HERK1/THE1 combination to attenuate salt effects, highlighting the complexity of the salt sensing mechanisms that rely on the cell wall integrity.
Soil salinity is an increasing worldwide problem for agriculture, affecting plant growth and yield. In our attempt to understand the molecular mechanisms activated in response to salt in plants, we investigated the Catharanthus roseus Receptor like Kinase 1 Like (CrRLK1L) family, which contains well described sensors previously shown to be involved in maintaining and sensing the structural integrity of the cell walls. We have observed that herk1the1-4 double mutants, lacking the function of the Arabidopsis thaliana Receptor like Kinase HERKULES1 combined with a gain of function allele of THESEUS1, phenocopied the phenotypes previously reported in plants lacking FERONIA (FER) function. We report that both fer-4 and herk1the1-4 mutants respond strongly to salt application, resulting in a more intense activation of early and late stress responses. We also show that salt triggers de-methyl esterification of loosely bound pectins. These cell wall modifications might be partly responsible for the activation of the signaling pathways required to activate salt stress responses. In fact, by adding calcium chloride or by chemically inhibiting pectin methyl esterase (PME) activity we observed reduced activation of the early signaling protein Mitogen Activated Protein Kinase 6 (MPK6) as well as a reduced amplitude in salt-induced marker gene induction. We show that MPK6 is required for the full induction of the salt-induced gene expression markers we tested. However, the sodium specific root halotropism response is likely regulated by a different branch of the pathway being independent of MPK6 or calcium application but influenced by the cell wall sensors FER/HERK1/THE1-4 and PME activity. We hypothesize a model where salt-triggered modification of pectin requires the functionality of FER alone or the HERK1/THE1 combination to attenuate salt responses. Collectively, our results show the complexity of salt stress responses and salt sensing mechanisms and their connection to cell wall modifications, likely being in part responsible for the response phenotypes observed in salt treated plants.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.