Biology subjects

Qi, L.

Publications and source records attributed to Qi, L..

At least 37 records · Page 2Linked to original sources

bioRxiv2025

Synergistic Control of Mitochondrial Dynamics and Function by ERAD and Autophagy in Brown Adipocytes

Mitochondrial quality control is essential for maintaining cellular energy homeostasis, particularly in brown adipocytes where dynamic mitochondrial remodeling supports thermogenesis. Although the SEL1L-HRD1 endoplasmic reticulum (ER)-associated degradation (ERAD) pathway and autophagy are two major proteostatic systems, how these pathways intersect to regulate mitochondrial integrity in metabolically active tissues remains poorly understood. Here, using adipocyte-specific genetic mouse models combined with high-resolution 2D and 3D ultrastructural imaging technologies, we reveal an unexpected synergy between SEL1L-HRD1 ERAD and autophagy in maintaining mitochondrial structure and function in brown adipocytes. Loss of ERAD alone triggers compensatory autophagy, whereas combined deletion of both pathways (double knockout, DKO) results in severe mitochondrial abnormalities, including the accumulation of hyperfused megamitochondria penetrated by ER tubules, even under basal room temperature conditions. These phenotypes are absent in mice lacking either pathway individually or in SEL1L-IRE1 DKO, highlighting the pathway-specific coordination between ERAD and autophagy. Mechanistically, dual loss of ERAD and autophagy induces ER expansion, excessive ER-mitochondria contact, upregulation of mitochondria-associated membrane (MAM) tethering proteins, impaired calcium transfer, and defective mitochondrial turnover. As a result, DKO adipocytes accumulate dysfunctional mitochondria, exhibit respiratory deficits, and fail to sustain thermogenesis. Collectively, our study uncovers a cooperative and previously unrecognized mechanism of mitochondrial surveillance, emphasizing the critical role of ERAD-autophagy crosstalk in preserving mitochondrial integrity and thermogenic capacity in brown fat. One-sentence summaryOur study uncovers a previously unrecognized synergy between SEL1L-HRD1 ERAD and autophagy that is essential for preserving mitochondrial integrity and thermogenic capacity in brown adipocytes, revealing new opportunities for targeting mitochondrial dysfunction in metabolic disease.

cell biology↗

bioRxiv2025

Modular Engineering of Escherichia coli for Enhanced Nickel Uptake, Survival, Biomineralization, and Hydrogen-Supported Bioremediation

Nickel contamination poses increasing environmental and industrial challenges, demanding effective and sustainable remediation strategies. Here, we present a modular synthetic biology approach to engineer Escherichia coli for efficient nickel enrichment, resilience in toxic environments, intracellular biomineralization, and hydrogen-based co-culture stability. Our system comprises four functional modules: (1) a nickel enrichment module, in which the fusion protein NixA-F1v outperformed existing uptake systems, and a mutant repressor RcnRC35L enhanced retention by suppressing nickel efflux; (2) a survival module where heterologous expression of Helicobacter pylori Hpn conferred tolerance to high nickel concentrations, and YejM increased phage resistance; (3) a nickel microparticle module enabling intracellular bioconversion of nickel into detectable microparticles even without engineered uptake proteins; and (4) a hydrogen supply module supporting co-culture stability through E. coli-cyanobacteria adhesion for sustained hydrogen production. These modules were experimentally validated through comparative uptake assays, survival profiling, and microscopy-based particle detection. Our findings demonstrate a customizable and integrative microbial platform for metal bioremediation and biosensing, with potential applications in environmental engineering and industrial waste treatment.

synthetic biology↗

bioRxiv2025

β-Arrestin Condensates Regulate G Protein-Coupled Receptor Function

G protein-coupled receptors (GPCRs) are the largest class of receptors in the genome and control many signaling cascades essential for survival. GPCR signaling is regulated by {beta}-arrestins, multifunctional adapter proteins that direct receptor desensitization, internalization, and signaling. While at many GPCRs, {beta}-arrestins interact with a wide array of signaling effectors, it is unclear how {beta}-arrestins promote such varied functions. Here we show that {beta}-arrestins undergo liquid-liquid phase separation (LLPS) to form condensates that regulate GPCR function. We demonstrate that {beta}-arrestin oligomerization occurs in proximity to the GPCR and regulates GPCR functions such as internalization and signaling. This model is supported by a cryoEM structure of the adhesion receptor ADGRE1 in a 2:2 complex with {beta}-arrestin 1, with a {beta}-arrestin orientation that can promote oligomerization. Our work provides a paradigm for {beta}-arrestin condensates as regulators of GPCR function, with LLPS serving as an important promoter of signaling compartmentalization at GPCRs.

cell biology↗

bioRxiv2025

SEL1L-HRD1 ER-Associated Degradation Facilitates Prohormone Convertase 2 Maturation and Glucagon Production in Islet α Cells

Proteolytic cleavage of proglucagon by prohormone convertase 2 (PC2) is required for islet cells to generate glucagon. However, the regulatory mechanisms underlying this process remain largely unclear. Here, we report that SEL1L-HRD1 endoplasmic reticulum (ER)-associated degradation (ERAD), a highly conserved protein quality control system responsible for clearing misfolded proteins from the ER, plays a key role in glucagon production by regulating turnover of the nascent proform of the PC2 enzyme (proPC2). Using a mouse model with SEL1L deletion in proglucagon-expressing cells, we observed a progressive decline in stimulated glucagon secretion and a reduction in pancreatic glucagon content. Mechanistically, we found that endogenous proPC2 is a substrate of SEL1L-HRD1 ERAD, and that degradation of misfolded proPC2 ensures the maturation of activation-competent proPC2 protein. These findings identify ERAD as a novel regulator of PC2 biology and an essential mechanism for maintaining cell function.

cell biology↗

bioRxiv2025

Phosphoproteomics Uncovers Tumor Heterogeneity and Therapeutic Opportunities in Early-Stage Hepatocellular Carcinoma

Mechanisms driving progression and metastasis in early-stage hepatocellular carcinoma (HCC) remain poorly clarified. Although phosphoproteomics has been applied to broader HCC cohorts, the heterogeneity of phosphorylation signaling in early-stage HCC remains unexplored. Here, we conducted integrated phosphoproteomic and proteomic analysis on early-stage HCC tumors and paired non-tumor tissues. By comparing tumor and non-tumor tissues, we identified markedly reduced phosphorylation of EGFR-mediated canonical ERK/MAPK signaling, alongside elevated atypical MAPK signaling in HCC. To further explore the signaling heterogeneity within tumors, we applied nonnegative matrix factorization (NMF) and consensus-clustering, and identified three distinct phosphoproteomic subtypes with unique phosphorylation signatures and clinical characteristics. Interrogating the most malignant subtype, we found markedly high abundance of phosphorylation of mRNA splicing regulators, and an enrichment of epithelial-mesenchymal transition (EMT) pathways in the proteome, with phosphorylation of the splicing factor SRSF3 emerging as a critical feature. Mechanistically, we show that SRSF3 hyperphosphorylation, driven by SRPK1/CLKs and potential PP1 phosphatase suppression, promotes metastasis and proliferation. Critically, SRPK1/CLKs inhibitors effectively suppressed SRSF3 hyperphosphorylation-mediated migration and invasion of HCC cells. Our study uncovers a new dimension of signaling-driven tumor heterogeneity in early-stage HCC and identifies the SRPK1/CLKs-SRSF3 hyperphosphorylation axis as a key metastatic driver, suggesting a potential therapeutic target for early intervention in HCC.

cancer biology↗

bioRxiv2024

Long-read sequencing reveals extensive size variation and suggests evolutionary patterns of expansion in bivalve mitogenomes

Bilaterian mitochondrial genomes are generally of conserved size and gene content, typically ranging from 14 to 20 kb and coding 37 genes. However, the major exception to this rule has been found in many bivalve species which allow the presence of long unassigned region (regions that are functionally unassigned). It is still unclear whether there are universal patterns to expansions across bivalves. Additionally, the prevalence of highly repetitive sequences within complex mitogenomes has prevented its complete assembly and led to its systematic omission from mitogenomic analyses. Here, leveraging the growing genomic resources in Mollusca, we devised a mitogenome assembly pipeline using long-read sequencing to characterize mitogenome features in 178 mollusk species. Comparing our assemblies with reference mitogenomes based on Sanger/short-read sequencing, we identified missing sequences, repeats and novel gene duplications and found that bivalves exhibit an exceptional diversity in mitogenome size compared to other mollusks. Subsequently, we investigated the factors potentially influencing mitogenome size, the potential functional elements and the patterns of expansion regions. Furthermore, we discussed that the possible selective pressure on mitogenome size and hypothesized that the variability of bivalve mitogenomes may be linked to innate immunity. Our findings underscore the significance of long-read sequencing in elucidating complex mitogenomes and provide new insights into the evolution of bivalve mitogenomes.

genomics↗

bioRxiv2024

Deciphering the Gut Microbiome's Influence on Depression: A Community-Level Constraint-Based Metabolic modelling Approach

BackgroundDepression is a common mental disorder worldwide, and its pathogenesis remains incompletely understood. However, increasing evidence suggests that gut microbiota play a significant role in the development of depression through the gut-brain-microbiota axis. However, due to the substantial individual variability in gut microbiota, while metabolic functions and metabolites between individuals are relatively similar, analyzing functional profiles and metabolic products yields more accurate results. ResultsIn this study, gut microbiota abundance data were collected from 354 depression patients and 5575 healthy individuals in the GMrepo v2 database. After matching for age and BMI, 271 paired samples from each group were retained. Alpha diversity analysis revealed significant differences between the two groups in the Observed, Shannon, and Chao1 indices, while beta diversity analysis indicated only subtle differences in gut microbiota composition. LEfSe analysis identified 23 differential species, with 18 enriched in the healthy group and 5 in the depression group. Further alpha diversity analysis of reaction abundance showed significant differences in the Observed and Chao1 indices, while beta diversity analysis did not reveal significant differences in reaction abundance. Differential and enrichment analyses identified 89 reactions that were significantly different between the groups, which were enriched in 4 metabolic pathways. Wilcoxon signed-rank test of COBRA-predicted metabolic fluxes revealed significant differences in the fluxes of 21 metabolites. Although the abundance of six species did not differ significantly between the two groups, their contributions to metabolic fluxes were significantly different. Mediation analysis indicated that gut microbiota influence the progression of depression by modulating various metabolites. ConclusionsThis study combined species abundance with COBRA metabolic flux predictions and mediation analysis, identified several differential species, as well as multiple differential metabolic fluxes, such as Cu2+ and L-Dopa, which were attributed to species like Dorea. Species such as Acholeplasma and Acidovorax were found to influence the progression of depression by affecting various metabolites, including Cu2+. These findings contribute to a deeper understanding of the relationship between gut microbiota and depression, offering new directions for the diagnosis and treatment of depression.

bioinformatics↗

bioRxiv2024

Mechanism of intestinal microbial metabolic flux disorder in hypertension

Hypertension is a major risk factor for cardiovascular diseases such as stroke and heart failure. Recent studies have shown that changes in the composition and function of the gut microbiota are closely related to the onset and development of hypertension. However, the individual differences in gut microbiota species make it difficult for traditional analysis methods to effectively reveal the pathogenic mechanisms of hypertension. In contrast, the inter-individual variability in gut microbial metabolites is much smaller, allowing for better cross-individual comparisons and reducing confounding factors in analysis. The interactions between gut microbiota and metabolites are highly complex, and network analysis can systematically capture this complexity. In this study Flux Balance Analysis (FBA) was utilized to predict the metabolic flux of gut microbiota and constructed cross-feeding networks. Random Forest and XGBoost models were employed to identify metabolites associated with hypertension. A differential microbial correlation network was used to analyze important metabolically related microbial sub-networks, and ultimately, the metabolic abnormalities and metabolite-related pathways were analyzed at the network level using the metabolite correlation network and cross-feeding networks. It was observed that the interaction patterns among 25 species--collectively referred to as the KEPR guild, with the most abundant genera being Eubacterium, Ruminococcus, Klebsiella, and Parabacteroides--changed, leading to alterations in 12 metabolites, such as choline (chol), 1-butanol (btoh), trimethylamine (tma), cytidine (cytd), and betaine (glyb) etc. Choline can be oxidized to form betaine, thereby affecting host blood pressure. Abnormalities in siroheme and methanethiol may result in reduced secretion of hydrogen sulfide by microbes, which in turn impacts blood pressure regulation mechanisms. The changes in these 12 metabolites may also enhance the degradation of mucin-type O-glycans and reduce butyrate metabolic activity, weakening the protective ability of intestinal epithelial cells. This may lead to inflammation and oxidative stress, exacerbating endothelial cell damage and consequently resulting in endothelial dysfunction and increased blood pressure. The findings of this study provide new insights into the pathogenic mechanisms of hypertension and offer potential targets for clinical intervention.

bioinformatics↗

bioRxiv2024

Systematic Mining of gut microbiota biomarkers for IBD

BackgroundInflammatory bowel disease (IBD), encompassing ulcerative colitis (UC) and Crohns disease (CD), represents a chronic inflammatory condition with an incompletely understood etiology. Emerging evidence suggests that alterations in gut microbiota composition play a pivotal role in disease development. Here, we leveraged gut fecal metagenomic data (3044 samples: 2248 IBD and 796 healthy) from publicly available sources to explore microbiome biomarkers related to IBD to provide new ideas for clinical treatment. ResultsOur analyses revealed marked disparities in microbial species abundance and composition between IBD and healthy samples in both male and female subjects from the United States, whereas such distinctions were absent in subjects from Spain. Hierarchical and systematic investigations uncovered microbial phyla, such as Verrucomicrobia and Firmicutes, associated with IBD in US cohorts. Furthermore, we identified 127 highly correlated pathways with these differential microbes, covering functions such as peptidoglycan biosynthesis III, dTDP-L-rhamnose biosynthesis I, starch degradation, and glucose-1-phosphate degradation. Gut microbial metabolites were predicted based on metagenomic data using the MelonnPan workflow and 16 metabolites with significant differences were identified that collectively contribute to energy metabolism, digestion, skin integrity and general bodily function. ConclusionsThis study identified differences in microbial species and metabolic pathways related to Inflammatory Bowel Disease (IBD) through hierarchical and systematic analysis, which can aid in the clinical diagnosis of IBD. Pathways such as Peptidoglycan Biosynthesis III and dTDP-L-Rhamnose Biosynthesis I are associated with the generation of bacterial cell walls, and disruptions in these pathways affect bacterial activity, leading to an imbalance in the hosts gut microbiota. Based on the hypotheses regarding the pathogenesis of IBD derived from the above mining results, it provides a theoretical basis for selecting precise treatment options.

bioinformatics↗

bioRxiv2024

Purkinje Cell-specific Deficiency in SEL1L-HRD1 Endoplasmic Reticulum-Associated Degradation Causes Progressive Cerebellar Ataxia in Mice

Recent studies have identified multiple genetic variants of SEL1L-HRD1 ER-associated degradation (ERAD) in humans with neurodevelopmental disorders and locomotor dysfunctions, including ataxia. However, the relevance and importance of SEL1L-HRD1 ERAD in the pathogenesis of ataxia remain unexplored. Here we show that SEL1L deficiency in Purkinje cells leads to early-onset progressive cerebellar ataxia with progressive loss of Purkinje cells with age. Mice with Purkinje cell-specific deletion of SEL1L (Sel1LPcp2Cre) exhibit motor dysfunction beginning around 9 weeks of age. Transmission electron microscopy (TEM) analysis reveals dilated ER and fragmented nuclei in Purkinje cells of adult Sel1LPcp2Cre mice, indicative of altered ER homeostasis and cell death. Lastly, loss of Purkinje cells is associated with a secondary neurodegeneration of granular cells, as well as robust activation of astrocytes and proliferation of microglia, in the cerebellum of Sel1LPcp2Cre mice. These data demonstrate the pathophysiological importance of SEL1L-HRD1 ERAD in Purkinje cells in the pathogenesis of cerebellar ataxia. One-sentence summarySEL1L-HRD1 ERAD is indispensable for Purkinje cell function and cerebellar ataxia pathogenesis in mice.

neuroscience↗

bioRxiv2024

Hierarchical global and local auxin signals coordinate cellular interdigitation in Arabidopsis

The development of multicellular tissues requires both local and global coordination of cell polarization, however, the mechanisms underlying their interplay are poorly understood. In Arabidopsis, leaf epidermal pavement cells (PC) develop a puzzle-piece shape locally coordinated through apoplastic auxin signaling. Here we show auxin also globally coordinates interdigitation by activating the TIR1/AFB-dependent nuclear signaling pathway. This pathway promotes a transient maximum of auxin at the cotyledon tip, which then moves across the leaf activating local PC polarization, as demonstrated by locally uncaged auxin globally rescuing defects in tir1;afb1;afb2;afb4;afb5 mutant but not in tmk1;tmk2;tmk3;tmk4 mutants. Our findings show that hierarchically integrated global and local auxin signaling systems, which respectively depend on TIR1/AFB-dependent gene transcription in the nucleus and TMK-mediated rapid activation of ROP GTPases at the cell surface, control PC interdigitation patterns in Arabidopsis cotyledons, revealing a mechanism for coordinating a local cellular process with the development of whole tissues.

plant biology↗

bioRxiv2024

Intra-genomic genes-to-genes correlation enables genome representaion

The bacterial pan-genome consists of core genes shared by all members of a taxonomy and accessory genes found in only a subset. The correlation among genes within the pan-genome could advance our understanding of evolution and tackle medical challenges. Here, we discovered a strong intra-genomic correlation among bacterial pan-genes within each of Escherichia coli, Listeria monocytogenes, Staphylococcus aureus, and Campylobacter jejuni. With a convolutional neural network assisted core genome knock-out simulation, we found that different combinations of fewer than 20 highly variable core genes could recover the sub-species type classified by complete core genome with accuracy >95%. This observation led us to test the genes-to-genes predictability: with more than 52,000 assemblies from each species, combinations of highly variable core genes could predict the sequence variants of other core genes (average accuracy >94%) within the same genome and could also predict sequence variants (average accuracy >91%) as well as the presence (average AUROC >0.91) of some accessory genes. Furthermore, combinations of highly variable core genes could also predict multiple antibiotic resistances (AUROC >0.80) in large published datasets of E. coli, S. aureus, and Mycobacterium tuberculosis. Collectively, we propose that genes within the same genome can strongly correlate with each other. Therefore, the strain phylogeny and the status of other genes could be uniformly represented by combinations of highly variable core genes, which could further represent certain phenotypes including in vitro resistance.

bioinformatics↗

bioRxiv2024

Extracellular electron transfer drives efficient H2-independent methylotrophic methanogenesis by Methanomassiliicoccus, a seventh order methanogen

Methylotrophic methanogenesis is achieved via methyl group dismutation or H2 reduction. This study reports extracellular electron droving efficient methylotrophic methanogenesis. The 7th order methanogen Methanomassiliicoccus luminyensis exclusively implements H2-dependent methylotrophic methanogenesis, but strain CZDD1 isolated from paddy soil possessed a higher methane-producing rate in coculture with Clostridium malenominatum CZB5 or the electrogenic Geobacter metallireducens. Chronoamperometry detected current production from CZB5, and current consumption accompanied CH4 production in a methanol-containing electrochemical culture of CZDD1. This demonstrated that M. luminyensis was capable of both direct species electron transfer (DIET) and extracellular electron transfer (EET) in methylotrophic methanogenesis. EET and DIET also enabled CZDD1 to produce methane from dimethyl arsenate. Differential transcriptomic analysis on H2-versus EET- and DIET-cocultures suggested that a membrane-bound Fpo-like complex and archaella of M. luminyensis CZDD1 could accept extracellular electrons. Given the ubiquitous environmental distribution of Methanomassiliicoccus strains, EET driven methylotrophic methanogenesis may contribute significantly to methane emission.

microbiology↗

bioRxiv2024

Platinum drug reprogramming of protein phosphorylation

Cisplatin is a DNA-targeting chemotherapeutic. Here we investigate how the cisplatin damaged gene loci are linked to specific protein-driven signalling pathways. Using forward chemical genetics methods, cisplatin damage to specific genes has been mapped in human lung cancer cells, a total of 16216 cisplatin-damaged genes (CDGs) with fold-enrichment > 1.5. Surprisingly, bioinformatics analysis demonstrates that cisplatin targets the majority of human protein kinase and phosphatase genes and involved in 300 core signalling pathways (-log p >4). The most associated key signalling pathways are sperm motility and protein kinase A. The highest related disease is cancer, and tissue toxicities related to CDGs are about hepato- and nephro- toxicities. Notably, cisplatin damaged 85% (440) of human protein kinase genes and 81% (110) of human protein phosphatase genes. This suggests that cisplatin acts as a multi-targeting protein-phosphorylation regulator, confirmed by a significant decrease in expression of a series of key protein kinase genes. These results reveal that cisplatin disrupts protein phosphorylation signalling genome-wide. Key points summarising the key messages of your articleA total of 16216 genes damaged by the clinical drug cisplatin in human lung cancer cells were identified using a forward chemical genetics method. Bioinformatics analysis revealed that cisplatin targets 85% of protein kinase and 81% of phosphatase genes. Cisplatin acts as a multi-targeting protein-phosphorylation regulator, disrupting protein phosphorylation signalling genome-wide. The disturbance of protein phosphorylation by cisplatin can be related to anticancer activity and tissue toxicities of the drug. These findings suggests novel strategies for rational design of next-generation anticancer metallodrugs involving specific targeting of protein phosphorylation.

cancer biology↗

bioRxiv2024

R-Loop Functions in Brca1-Associated Mammary Tumorigenesis

Excessive R-loops, a DNA-RNA hybrid structure, are associated with genome instability and BRCA1 mutation-related breast cancer. Yet the causality of R-loops in tumorigenesis remains unclear. Here we show that R-loop removal by Rnaseh1 overexpression (Rh1-OE) in Brca1-knockout (BKO) mouse mammary epithelium exacerbates DNA replication stress without affecting homology-directed DNA repair. R-loop removal also diminishes luminal progenitors, the cell of origin for estrogen receptor (ER)-negative BKO tumors. However, R-loop reduction does not dampen spontaneous BKO tumor incidence. Rather, it gives rise to a significant percentage of ER-expressing BKO tumors. Thus, R-loops reshape mammary tumor subtype rather than promoting tumorigenesis.

cancer biology↗

bioRxiv2024

IL-1beta-induced epithelial cell and fibroblast transdifferentiation fuels neutrophil recruitment in chronic rhinosinusitis with nasal polyps

Neutrophilic inflammation contributes to multiple chronic inflammatory airway diseases, including asthma and chronic rhinosinusitis with nasal polyps (CRSwNP), and is associated with an unfavorable prognosis. Here, using single-cell RNA sequencing (scRNA-seq) to profile human nasal mucosa obtained from the inferior turbinates, middle turbinates, and nasal polyps of CRSwNP patients, we identified two IL-1 signaling-induced cell subsets--LY6D+ club cells and IDO1+ fibroblasts--that promote neutrophil recruitment by respectively releasing S100A8/A9 and CXCL1/2/3/5/6/8 into inflammatory regions. IL-1{beta}, a pro-inflammatory cytokine involved in IL-1 signaling, induces the transdifferentiation of LY6D+ club cells and IDO1+ fibroblasts from primary epithelial cells and fibroblasts, respectively. In an LPS-induced neutrophilic CRSwNP mouse model, blocking IL-1{beta} activity with a receptor antagonist significantly reduced the numbers of LY6D+ club cells and IDO1+ fibroblasts and mitigated nasal inflammation. This study reveals the roles of two cell subsets in neutrophil recruitment and demonstrates an IL-1-based intervention for mitigating neutrophilic inflammation in CRSwNP.

immunology↗

bioRxiv2023

Guanylate cyclase activity of TIR1/AFB auxin receptorsin rapid auxin responses

The plant hormone auxin is perceived by TIR1/AFB receptors, which mediate transcriptional reprogramming via a ubiquitination- and cAMP-dependent mechanism. Same receptors mediate also rapid, non-transcriptional growth responses that are mechanistically less well understood. Here, we demonstrate that TIR1/AFB receptors possess not only adenylate cyclase but also guanylate cyclase activity. Auxin perception independently activates cAMP and cGMP production by TIR1/AFBs in vitro and elevates both cAMP and cGMP levels in planta. Genetic and synthetic biology approaches revealed that AFB1 guanylate cyclase activity is required for the rapid cytosolic Ca2+ transients and root growth inhibition. This unprecedented combination of adenylate and guanylate cyclase activities within a single hormone receptor establishes a new paradigm for how one perception mechanism can mediate distinct downstream responses. One-Sentence SummaryTIR1/AFB auxin receptors possess both, adenylate and guanylate cyclase activities, mediating transcriptional reprogramming and rapid Ca2+-dependent growth responses, respectively.

plant biology↗

bioRxiv2023

MdHY5 and MdHY5S form a transcription loop to regulate browning and phenolics synthesis in apple under purple light

Enzymatic browning significantly affects the appearance and quality of fresh-cut fruit. Light treatment can effectively inhibit fresh-cut apple browning via unknown molecular mechanisms. Here, we found that the application of purple LED light decreased the browning index of fresh-cut apple, delaying browning as compared to that of fresh-cut apple placed in the dark, and suggesting that purple LED light suppresses browning. In addition, the expression levels of MdHY5 and MdHY5S, important BASIC LEUCINE ZIPPER DOMAIN (bZIP) transcription factors that are involved in the light signaling pathway, were increased by purple LED light treatment. Silencing MdHY5 and MdHY5S in apple meant that purple LED light treatment no longer inhibited fresh-cut apple browning, the expression levels of the browning-related genes POLYPHENOL OXIDASE (MdPPO) and PEROXIDASE (MdPOD) increased, and the expression of the phenolic synthesis gene PHENYLALANINE AMMONIALYASE (MdPAL) decreased. Further study revealed that MdHY5 and MdHY5S bind to the MdPPO and MdPOD promoters, reducing their transcription. In contrast, MdHY5 and MdHY5S bind to the MdPAL promoter, enhancing transcription. Further research revealed that MdHY5 and MdHY5S also bind directly to each others promoters to form a positive transcriptional loop that activates their transcription. Our findings revealed that purple LED light inhibits browning and increases phenolics synthesis in fresh-cut apple by activating MdHY5 and MdHY5S. The results provide a theoretical basis upon which the new methods for improving the appearance and quality of fresh-cut apple can be based.

developmental biology↗