Biology subjects

Liu, C.-J.

Publications and source records attributed to Liu, C.-J..

7 recordsLinked to original sources

bioRxiv2025

Emergence of Lignin-Carbohydrate Interactions During Plant Stem Maturation Visualized by Solid-State NMR

Lignification waterproofs and strengthens the secondary plant cell wall, while increasing the energy cost associated with releasing sugars for biofuel production. The physical association between lignin and the carbohydrate scaffold that accommodates lignin polymerization, as well as the temporally distinct roles of different lignin units and carbohydrate partners during lignification, remain largely unclear. Here we map the lignin-carbohydrate interactions by solid-state NMR in 13C-labeled Arabidopsis inflorescence stems as secondary cell walls are formed. Analysis includes wild-type and two mutants that either selectively or globally disrupt lignin biosynthesis. Mature cell walls in the basal regions of older stems are enriched in S-lignin and carbohydrate-lignin interactions. Acetylated xylan is the dominant mediator of interactions with S-lignin, while methylated pectin unexpectedly interacts with G-lignin during early-stage lignification. The critical role of S-lignin in stabilizing carbohydrate-lignin interface is emphasized by the weak lignin-carbohydrate interactions and compromised mechanical properties of a low-S fah1 mutant, whereas the ref3 mutant, with low overall lignin content but a higher S/G ratio, remained unaffected. These findings demonstrate that the molecular mixing pattern, rather than lignin content, is a key determinant of the structure and properties of lignocellulosic materials.

biophysics↗

bioRxiv2024

Iron deprivation activates aboveground cell wall biosynthesis in Populus and the role of PtrbHLH011

Lack of mechanistic understanding of the environmental plasticity of secondary cell wall (SCW) biosynthesis hinders the massive bioenergy production on marginal lands. Growing bioenergy crops on marginal lands is appealing to minimize competition for arable land. However, abiotic stresses, particularly iron deficiency stress, are widespread to perturb SCW biosynthesis. In poplar, a major bioenergy crop, we demonstrated that iron deprivation activates stem SCW biosynthesis and identified transcription factor PtrbHLH011 as a possible underlying regulator. PtrbHLH011 is a potent repressor of SCW, whose overexpression resulted in a reduction of stem SCW by over 65%. Our genomic and molecular studies discovered that PtrbHLH011 binds to the AAAGACA sequence and represses essential genes for SCW biosynthesis, flavonoid biosynthesis, and iron homeostasis. Wood formation and iron deprivation downregulates PtrbHLH011 to release the transcriptional repression. Our findings reveal a regulatory mechanism coordinating SCW biosynthesis in response to environmental iron availability and suggest that PtrbHLH011 manipulation may help engineer bioenergy crops with improved performance under marginal conditions.

plant biology↗

bioRxiv2023

Continuity of Mitochondrial Budding: Insights from BS-C-1 Cells by in-situ Cryo-Electron Tomography

Mitochondrial division is a fundamental biological process that is crucial to cellular functionality and vitality. The prevailing hypothesis of Drp1 regulation with the involvement of ER and cytoskeleton does not account for all the observations. Following up our previous study in HeLa cells which led to the new hypothesis of mitochondrial division by budding, we employed in-situ Cryo-Electron Tomography (Cryo-ET) to visualize mitochondrial budding in intact healthy monkey kidney cells (BS-C-1 cells). Our findings reaffirm single and multiple mitochondrial budding, supporting the new hypothesis. Notably, the budding regions vary significantly in diameter and length, which may represent different stages of budding. More interestingly, no rings, or ring-like structures, or ER wrapping is presented in the budding regions suggesting mitochondrial budding is independent from Drp1 and ER. Meanwhile, we uncovered direct interactions between mitochondria and large vesicles, distinct from small mitochondrial-derived vesicles and extracellular mitovesicles. We propose these interacting vesicles may have mitochondrial origins.

biophysics↗

bioRxiv2023

Functional specialization of cytochrome b5 prior to the invention of syringyl lignin biosynthesis

The production of lignin represents a hallmark of vascular plant evolution. But syringyl-lignin production is lineage specific. Its emergence in angiosperms has been regarded as a recent evolution event, as is the appearance of syringyl monomer biosynthetic F5H (CYP84A1). Angiosperm F5H uniquely requires cytochrome b5 protein CB5D as an obligatory redox partner. However, it remains unclear how CB5D functionally evolved and specialized and whether it co-evolved with F5H. Here we show that plant CB5 family expanded and functionally specialized at the early stage of plant terrestrialization. CB5D was absent in green algae but emerged in bryophytes and conserved in most embryophytes, particularly proliferating in angiosperms. The innovation of CB5D is attributed to the evolution and maintenance of acidic amino residues in the helix 5 of CB5 protein. Interestingly, the syringyl-lignin producing lycophyte Selaginella lacks the functionally specialized CB5D. The Selaginella F5H (CYP788A1) solely relies on cytochrome P450 reductase as a redox partner. These results suggest that CB5 functionally diversified and specialized prior to the divergence of land plant lineages but lost in Selaginella; and the recently evolved angiosperm F5H has co-opted the anciently invented CB5D to form a modern cytochrome P450 monooxygenase system enabling the re-emergence of syringyl-lignin biosynthesis in higher plants. One Sentence SummaryCytochrome b5 D, an indispensable electron donor for F5H-catalyzed S-lignin biosynthesis, was invented prior to the divergence of land plant lineages, earlier than the emergence of vascular plant F5Hs.

plant biology↗

bioRxiv2022

Novel Peptide Inhibitor of Human Tumor Necrosis Factor-α has Antiarthritic Activity

The inhibition of tumor necrosis factor- (TNF) trimer formation renders it inactive for binding to its receptors thus mitigating the vicious cycle of inflammation. We designed a peptide (PIYLGGVFQ) that simulates a sequence strand of human TNF monomer using a series of in silico methods, such as active site finding (Acsite), protein-protein interaction (PPI), docking studies (GOLD and Modeller) followed by molecular dynamics (MD) simulation studies. The MD studies confirmed the intermolecular interaction of the peptide with the TNF. Fluorescence-activated cell sorting (FACS) and fluorescence microscopy revealed that the peptide effectively inhibited the binding of TNF to the cell surface receptors. The cell culture assays showed that the peptide significantly inhibited the TNF-mediated cell death. In addition, the nuclear translocation of the nuclear factor kappa B (NF{kappa}B) was significantly suppressed in the peptide-treated A549 cells as observed in immunofluorescence and gel mobility-shift assays. Furthermore, peptide protected against joint damage in collagen-induced arthritis (CIA) mouse model as revealed in the microfocal-CT scans. In conclusion, this TNF antagonist would be useful for the prevention and repair of inflammatory bone destruction and subsequent loss in the mouse model of CIA as well as human rheumatoid arthritis (RA) patients. This calls upon further clinical investigation to utilize its potential effect as an anti-arthritic drug.

immunology↗

bioRxiv2019

An ultra-sensitive T-cell receptor detection method for TCR-Seq and RNA-Seq data

T-cell receptors (TCRs) recognizing antigens play vital roles in T-cell immunology. Surveying TCR repertoires by characterizing complementarity-determining region 3 (CDR3) can provide valuable insights into the immune community underlying pathologic conditions, which will benefit neoantigen discovery and cancer immunotherapy. Here we present a novel tool named CATT, which can apply on TCR sequencing (TCR-Seq), RNA-Seq, and single-cell TCR(RNA)-Seq data to characterize CDR3 repertoires. CATT integrated maximum-network-flow based micro-assembly algorithm, data-driven error correction model, and Bayes classification algorithm, to self-adaptively and ultra-sensitively characterize CDR3 repertoires with high accuracy. Benchmark results of datasets from in silico and real conditions demonstrated that CATT showed superior recall and precision compared with other prevalent tools, especially for datasets with short read length and small data size. By applying CATT on a TCR-Seq dataset from aplastic anemia patients, we found the skewing of TCR repertoire was due to the oligoclonal expansion of effector memory T-cells. CATT will be a powerful tool for researchers conducting TCR and immune repertoire studies. CATT is freely available at http://bioinfo.life.hust.edu.cn/CATT.

bioinformatics↗

bioRxiv2019

Glucosinolate and phenylpropanoid biosynthesis are linked by proteasome-dependent degradation of PAL

Plants produce several hundreds of thousands of secondary metabolites that are important for adaptation to various environmental conditions. Although different groups of secondary metabolites are synthesized through unique biosynthetic pathways, plants must orchestrate their production simultaneously.\n\nPhenylpropanoids and glucosinolates are two classes of secondary metabolites that are synthesized through apparently independent biosynthetic pathways. Genetic evidence has revealed that the accumulation of glucosinolate intermediates limits phenylpropanoid production in a Mediator Subunit 5 (MED5) dependent manner.\n\nTo elucidate the molecular mechanism underlying this process, we analyzed the transcriptomes of a suite of glucosinolate-deficient mutants using RNAseq and identified mis-regulated genes that are rescued by the disruption of MED5. The expression of a group of Kelch Domain F-Box genes (KFBs) that function in PAL degradation is affected in glucosinolate biosynthesis mutants and the disruption of these KFBs restores phenylpropanoid deficiency, dwarfism and sterility in the mutants.\n\nOur study suggests that glucosinolate/phenylpropanoid metabolic crosstalk involves the transcriptional regulation of KFB genes that initiate the degradation of the enzyme phenylalanine ammonia-lyase, which catalyzes the first step of the phenylpropanoid biosynthesis pathway. Nevertheless, KFB mutant plants remain partially sensitive to glucosinolate pathway mutations, suggesting that other mechanisms that link the two pathways also exist.

plant biology↗