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Salt stress is a major environmental stress that affects plant growth and development. Plants are sessile and thus have to develop suitable mechanisms to adapt to high-salt environments. Salt stress increases the intracellular osmotic pressure and can cause the accumulation of sodium to toxic levels. Thus, in response to salt stress signals, plants adapt via various mechanisms, including regulating ion homeostasis, activating the osmotic stress pathway, mediating plant hormone signaling, and regulating cytoskeleton dynamics and the cell wall composition. Unraveling the mechanisms underlying these physiological and biochemical responses to salt stress could provide valuable strategies to improve agricultural crop yields. In this review, we summarize recent developments in our understanding of the regulation of plant salt stress.

Due to their bacterial ancestry, many components of mitochondria share structural similarities with bacteria. Release of molecular danger signals from injured cell mitochondria (mitochondria-derived damage-associated molecular patterns, mito-DAMPs) triggers a potent inflammatory response, but their role in fibrosis is unknown. Using liver fibrosis resistant/susceptible mouse strain system, we demonstrate that mito-DAMPs released from injured hepatocyte mitochondria (with mtDNA as major active component) directly activate hepatic stellate cells, the fibrogenic cell in the liver, and drive liver scarring. The release of mito-DAMPs is controlled by efferocytosis of dying hepatocytes by phagocytic resident liver macrophages and infiltrating Gr-1(+) myeloid cells. Circulating mito-DAMPs are markedly increased in human patients with non-alcoholic steatohepatitis (NASH) and significant liver fibrosis. Our study identifies specific pathway driving liver fibrosis, with important diagnostic and therapeutic implications. Targeting mito-DAMP release from hepatocytes and/or modulating the phagocytic function of macrophages represents a promising antifibrotic strategy. Progressive fibrosis is a driver of morbidity and mortality in many chronic liver diseases, but the underlying mechanisms are incompletely understood. Here, the authors show that mitochondria-derived damage-associated molecular patterns are released from injured hepatocytes and can trigger fibrogenic activation of hepatic stellate cells.

As the stimulus-responsive mediator of actin dynamics, actin-depolymerizing factor (ADF)/cofilin is subject to tight regulation. It is well known that kinase-mediated phosphorylation inactivates ADF/cofilin. Here, however, we found that the activity of Arabidopsis ADF7 is enhanced by CDPK16-mediated phosphorylation. We found that CDPK16 interacts with ADF7 both in vitro and in vivo , and it enhances ADF7-mediated actin depolymerization and severing in vitro in a calcium-dependent manner. Accordingly, the rate of actin turnover is reduced in cdpk16 pollen and the amount of actin filaments increases significantly at the tip of cdpk16 pollen tubes. CDPK16 phosphorylates ADF7 at Serine128 both in vitro and in vivo , and the phospho-mimetic mutant ADF7 S128D has enhanced actin-depolymerizing activity compared to ADF7. Strikingly, we found that failure in the phosphorylation of ADF7 at Ser128 impairs its function in promoting actin turnover in vivo , which suggests that this phospho-regulation mechanism is biologically significant. Thus, we reveal that CDPK16-mediated phosphorylation up-regulates ADF7 to promote actin turnover in pollen.

The opening and closing of stomata are crucial for plant photosynthesis and transpiration. Actin filaments undergo dynamic reorganization during stomatal closure, but the underlying mechanism for this cytoskeletal reorganization remains largely unclear. In this study, we identified and characterized Arabidopsis thaliana casein kinase 1-like protein 2 (CKL2), which responds to abscisic acid (ABA) treatment and participates in ABA- and drought-induced stomatal closure. Although CKL2 does not bind to actin filaments directly and has no effect on actin assembly in vitro, it colocalizes with and stabilizes actin filaments in guard cells. Further investigation revealed that CKL2 physically interacts with and phosphorylates actin depolymerizing factor 4 (ADF4) and inhibits its activity in actin filament disassembly. During ABA-induced stomatal closure, deletion of CKL2 in Arabidopsis alters actin reorganization in stomata and renders stomatal closure less sensitive to ABA, whereas deletion of ADF4 impairs the disassembly of actin filaments and causes stomatal closure to be more sensitive to ABA. Deletion of ADF4 in the ckl2 mutant partially recues its ABA-insensitive stomatal closure phenotype. Moreover, Arabidopsis ADFs from subclass I are targets of CKL2 in vitro. Thus, our results suggest that CKL2 regulates actin filament reorganization and stomatal closure mainly through phosphorylation of ADF.

Although it is well established that the Polycomb Group (PcG) complexes maintain gene repression through the incorporation of H2AK121ub and H3K27me3, little is known about the effect of these modifications on chromatin accessibility, which is fundamental to understand PcG function. Here, by integrating chromatin accessibility, histone marks and expression analyses in different Arabidopsis PcG mutants, we show that PcG function regulates chromatin accessibility. We find that H2AK121ub is associated with a less accessible but still permissive chromatin at transcriptional regulation hotspots. Accessibility is further reduced by EMF1 acting in collaboration with PRC2 activity. Consequently, H2AK121ub/H3K27me3 marks are linked to inaccessible although responsive chromatin. In contrast, only-H3K27me3-marked chromatin is less responsive, indicating that H2AK121ub-marked hotspots are required for transcriptional responses. Nevertheless, despite the loss of PcG activities leads to increased chromatin accessibility, this is not necessarily accompanied by transcriptional activation, indicating that accessible chromatin is not always predictive of gene expression. Polycomb Group complexes maintain gene repression through the incorporation of H2AK121ub and H3K27me3. Here, the authors show that H2AK121ub marks less accessible but transcriptionally permissive chromatin, while H3K27me3 enforces a repressed transcriptionally less-permissive state.

Salt stress is a major challenge to agricultural productivity and can adversely affect plant growth and development. This review examines the interaction between cell wall architecture and plant tolerance to salt stress, focusing on the mechanisms underlying growth, remodeling, and anisotropic morphogenesis. It further elucidates how the cell wall’s composition, structure, and mechanical properties affect osmotic balance, ion transport, and physiological responses to salinity in plants. Key strategies for adaptation to stress, including the synthesis of osmoprotectants and alterations in cell wall polysaccharides, are discussed to understand their role in cell integrity and expansion under salt conditions. In addition, the review emphasizes the dynamic remodeling of the cell wall, which promotes anisotropic growth patterns necessary to maintain plant structure and function under environmental stresses. Based on the current research, this review highlights potential pathways to enhance plant adaptation to salinity through targeted manipulation of cell wall properties, providing insights for future biotechnological applications to improve crop performance in a saline environment.

The elimination of seed shattering was a crucial event during crop domestication. Improving and fine-tuning the regulation of this process will further enhance grain yield by avoiding seed losses during crop production. In this work, we identified the loss-of-shattering mutant suppression of shattering1 (ssh1) through a screen of mutagenized wild rice (Oryza rufipogon) introgression lines with naturally high shattering. Using the MutMap approach and transformation experiments, we isolated a genetic factor for seed shattering, SSH1, which is an allele of SUPERNUMERARY BRACT (SNB), a gene encoding a plant-specific APETALA2-like transcription factor. A C-to-A point mutation in the ninth intron of SNB altered the splicing of its messenger RNA, causing the reduced shattering of the ssh1 mutant by altering the development of the abscission layer and vascular bundle at the junction between the seed and the pedicel. Our data suggest that SNB positively regulates the expression of two rice REPLUMLESS orthologs, qSH1 and SH5. In addition, the ssh1 mutant had larger seeds and a higher grain weight, resulting from its increased elongation of the glume longitudinal cells. The further identification of favorable SNB alleles will be valuable for improving rice seed shattering and grain yield using molecular breeding strategies.

Background Anlotinib is a multi-target tyrosine kinase inhibitor (TKI) targeting the vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), fibroblast growth factor receptor (FGFR), and c-Kit. This phase II study aimed to assess the efficacy and safety of anlotinib, either alone or in combination with bevacizumab (Bev) for recurrent high-grade glioma (rHGG) (NCT04822805, 30/03/2021). Methods Eligible patients had a histological diagnosis of rHGG with first or subsequent recurrences. All patients received oral anlotinib 12 mg or 10 mg on days 1–14 (repeated every 21 days). In cases where brain magnetic resonance imaging examination revealed an increase in peritumoral edema without worsening of symptoms, patients received a temporary treatment of intravenous bevacizumab 10 mg/kg to alleviate edema. The primary endpoint was the median progression-free survival (mPFS), and the secondary endpoints included median overall survival (mOS), objective response rate (ORR), disease control rate (DCR), and safety. Results Twenty-five patients with rHGG were included in the efficacy and safety assessments. Eighteen patients received anlotinib alone, and seven patients received anlotinib in combination with Bev. For all patients, the mPFS and mOS were 5.0 months and 13.6 months, respectively. The ORR was 32%, and the DCR was 96%. It is noteworthy that the survival and response data of recurrent glioblastoma (rGBM) exhibit similarities to those of rHGG. For rGBM patients, there were no significant differences in mPFS, mOS, ORR, or DCR between the anlotinib alone and anlotinib + Bev groups. However, the incidence of treatment-related adverse events of any grade was higher in the anlotinib + Bev group compared to the anlotinib alone group (100% vs. 78%, p  = 0.041). Conclusions Both anlotinib alone and its combination with Bev demonstrated good efficacy and safety in the treatment of rHGG.

The terrible morbidity and mortality of malignant tumors urgently require innovative therapeutics, especially for apoptosis‐resistant tumors. Pyroptosis, a pro‐inflammatory form of programmed cell death (PCD), is featured with pore formation in plasma membrane, cell swelling with giant bubbles, and leakage of cytoplasmic pro‐inflammatory cytokines, which can remodel the tumor immune microenvironment by stimulating a “cold” tumor microenvironment to be an immunogenic “hot” tumor microenvironment, and consequently augment the therapeutic efficiency of malignant tumors. Benefiting from current advances in nanotechnology, nanomedicine is extensively applied to potentiate, enable, and augment pyroptosis for enhancing cancer‐therapeutic efficacy and specificity. This review provides a concentrated summary and discussion of the most recent progress achieved in this emerging field, highlighting the nanomedicine‐enabled/augmented specific pyroptosis strategy for favoring the construction of next‐generation nanomedicines to efficiently induce PCD. It is highly expected that the further clinical translation of nanomedicine can be accelerated by inducing pyroptotic cell death based on bioactive nanomedicines. Nanomedicine‐induced pyroptosis for efficient tumor therapeutics is increasingly prominent at current stage. This review provides a comprehensive summary and deep discussion on the very‐recent progress achieved in this emerging field.

Improving the yield by modifying plant architecture was a key step during crop domestication. Here, we show that a 110-kb deletion on the short arm of chromosome 7 in Asian cultivated rice ( Oryza sativa ), which is closely linked to the previously identified PROSTRATE GROWTH 1 ( PROG1 ) gene, harbors a tandem repeat of seven zinc-finger genes. Three of these genes regulate the plant architecture, suggesting that the deletion also promoted the critical transition from the prostrate growth and low yield of wild rice ( O . rufipogon ) to the erect growth and high yield of Asian cultivated rice. We refer to this locus as RICE PLANT ARCHITECTURE DOMESTICATION ( RPAD ). Further, a similar but independent 113-kb deletion is detected at the RPAD locus in African cultivated rice. These results indicate that the deletions, eliminating a tandem repeat of zinc-finger genes, may have been involved in the parallel domestication of plant architecture in Asian and African rice. Plant architecture transition is one of the great consequences during rice domestication. Here, the authors find that chromosomal deletions linked to the previously known PROG1 gene also participate in plant architecture domestication in both Asian and African cultivated rice.