Biology subjects

Ji, W.

Publications and source records attributed to Ji, W..

At least 37 records · Page 2Linked to original sources

bioRxiv2024

Sec14L6 is a PS and PI4P transporter that promotes lipid droplet formation

Lipid droplets (LDs) are evolutionarily conserved organelles that are crucial for cellular metabolism. LD biogenesis and growth occurs in the ER and requires the supply of phospholipid from the ER, but the molecular basis is largely unclear. Here, we have identified Sec14L6, a unique protein of the Sec14 family, as a PS/PI4P transporter required for LD biogenesis. Sec14L6 knockout (KO) greatly reduces the number of LDs that can be rescued by wild-type rather than lipid transfer-defective Sec14L6 mutants. We found that Sec14L6 directly interacts with ACSL3, and that this interaction facilitates targeting of Sec14L6 to LDs and activates the PS transfer activity of Sec14L6 in vitro. We also identified PGRMC1, an ER membrane protein, as an adaptor that recruits Sec14L6 to the ER. Furthermore, depletion of Sec14L6 impairs differentiation of adipose-derived mesenchymal stem cells. Together, our study suggests that Sec14L6 transports PS and/or PI4P between the ER and LDs to promote LD formation.

cell biology↗

bioRxiv2024

Intra-subgenome regulation induces unbalanced expression and function among bread wheat homoeologs

The differential expression of homoeologous genes confers expression plasticity and facilitates the adaptation and domestication of major polyploid crops. However, how this homoeolog expression bias (HEB) is regulated remains elusive. Here, transcriptome analysis of 406 wheat (Triticum aestivum; AABBDD) accessions revealed great variation in HEB among accessions. We identified 14,727 QTLs regulating HEB (hebQTLs), indicating that HEB is genetically regulated and can be predicted using genotyping data. The hebQTLs only regulate the expression of homoeologs in the same subgenome and downregulate their expression to result in HEB, suggesting that intra-subgenomic rather than inter-subgenomic interactions induce HEB. Furthermore, non-hebQTL-regulated homoeologs have stronger biological functions, are under higher selection pressure and exhibit lower genetic diversity than hebQTL-regulated homoeologs and compensate for the downregulated expressions of hebQTL-regulated homoeologs. Our findings reveal how homoeolog expression is coordinated at the genetic level and provide an avenue for leveraging HEB to improve polyploid crops.

genomics↗

bioRxiv2024

Integrated single-cell RNA-seq analysis revealed PTN secreted by fibroblasts acting on itself and macrophages via SDC4 ligand in myocardial hypertrophy

BackgroundHypertrophic cardiomyopathy (HCM) is characterized by massive myocardial hypertrophy, which is the most frequent cause of sudden death and can lead to heart failure (HF) or stroke. The objective of this study was to explore the communication network among various cells in the heart of pathological HCM derived from transverse aortic constriction (TAC) mouse model, and investigate the potential mechanism through data mining, biological informatics analysis, and experimental validation. Methods and ResultsThe integrated analyses including CellChat, Seurat, gene ontology (GO), pseudo-time trajectory analysis, and weighted gene co-expression network analysis (WGCNA) were performed based on the single-cell RNA-seq data (scRNA-seq). In vitro tests were conducted to verify bioinformatic analysis findings through enzyme-linked immunosorbent assay (ELISA), real-time quantitative PCR (RT-qPCR), Edu staining, and transwell assay. In vivo tests were also performed to further verify bioinformatic analysis findings by western blot and immunofluorescence assays based on our established TAC mouse model with myocardial hypertrophy. Our results showed that in the heart of TAC mouse, the interaction between cardiac fibroblasts and macrophages was most common, and the increasing pleiotrophin (PTN) secreted by cardiac fibroblasts could promote themselves proliferation or invasion as well as stimulate macrophage activation to release inflammatory cytokines, such as TNF-, IL-6, Cox-2, Cd83, Egr2, and IL-10 through acting on its ligand recombinant Syndecan 4 (SDC4), which may affect cardiomyocyte normal function and eventually cause HCM. This study first demonstrated that PTN derived from cardiac fibroblasts may act on SDC4 to play crucial role in myocardial hypertrophy, which may be a potential therapeutic targets for patients with pathological HCM. ConclusionsIn this study, the complex interaction network between cardiac fibroblasts and macrophages of TAC mice based on the scRNA-seq data was investigated, and we found that the increasing PTN secreted by cardiac fibroblasts under cardiac pressure overload could promote themselves proliferation or invasion as well as stimulate macrophage activation to release inflammatory cytokines through acting on SDC4 ligand, which may affect cardiomyocyte normal function and eventually cause HCM. In addition, our study suggested that PTN derived from cardiac fibroblasts may act on SDC4 ligand to play crucial role in myocardial hypertrophy, which may be a potential therapeutic targets for patients with pathological HCM.

cell biology↗

bioRxiv2024

A single mutation in dairy cow-associated H5N1 viruses increases receptor binding breadth

Clade 2.3.4.4b H5N1 is causing an unprecedented outbreak in dairy cows in the United States. To understand if recent H5N1 viruses are changing their receptor use, we screened recombinant hemagglutinin (HA) from historical and recent 2.3.4.4b H5N1 viruses for binding to distinct glycans bearing terminal sialic acids. We found that H5 from A/Texas/37/2024, an isolate from the dairy cow outbreak, has increased binding breadth to glycans bearing terminal 2,3 sialic acids, the avian receptor, compared to historical and recent 2.3.4.4b H5N1 viruses. We did not observe any binding to 2,6 sialic acids, the receptor used by human seasonal influenza viruses. We identified a single mutation outside of the receptor binding site, T199I, was responsible for increased binding breadth, as it increased receptor binding site flexibility. Together, these data show recent H5N1 viruses are evolving increased receptor binding breadth which could impact the host range and cell types infected with H5N1.

microbiology↗

bioRxiv2024

CAMSAP3 Forms Dimers via its lapha-helix Domain that Directly Stabilize Non-centrosomal Microtubule Minus Ends

Microtubules are vital components of the cytoskeleton. Their plus ends are dynamic and respond to changes in cell morphology, while the minus ends are stable and serve a crucial role in microtubule seeding and maintaining spatial organization. In mammalian cells, the calmodulin-regulated spectrin-associated proteins (CAMSAPs), play a key role in directly regulating the dynamics of non-centrosomal microtubules minus ends. However, the molecular mechanisms are not yet fully understood. Our study reveals that CAMSAP3 forms dimers through its C-terminal -helix; this dimerization not only enhances the microtubule-binding affinity of the CKK domain but also enables the CKK domain to regulate the dynamics of microtubules. Furthermore, CAMSAP3 also specializes in decorating at the minus end of microtubules through the combined action of the microtubule-binding domain (MBD) and the C-terminal -helix, thereby achieving dynamic regulation of the minus ends of microtubules. These findings are crucial for advancing our understanding and treatment of diseases associated with non-centrosomal microtubules. SignificanceOur study reveals the molecular mechanism of how CAMSAP3, a key regulator of non-centrosomal microtubule dynamics, directly regulates the dynamics of non-centrosomal microtubule minus ends through CKK domain. CAMSAP3 forms dimers through its C-terminal -helix, which enhances the CKK domain of CAMSAP3 binding to microtubule minus ends and confers stability of them. This finding is not limited to CAMSAP3, but can also be applied to the understanding of the regulation of non-centrosomal microtubule minus end stability by CAMSAP family proteins. Our findings deepen our comprehension of cellular structure and function, offering insights into the role of microtubules in cellular integrity and disease. This study fills a significant knowledge gap and lays the foundation for future research into the complex balance of microtubule dynamics required for cellular health and disease prevention.

cell biology↗

bioRxiv2024

The protective roles of Eugenol on type 1 diabetes mellitus through NRF2 mediated oxidative stress pathway

Type 1 diabetes mellitus (T1DM), known as insulin-dependent diabetes mellitus, is characterized by persistent hyperglycemia resulting from damage to the pancreatic {beta} cells and an absolute deficiency of insulin, leading to multi-organ involvement and a poor prognosis. The progression of T1DM is significantly influenced by oxidative stress and apoptosis. The natural compound eugenol (EUG) possesses anti-inflammatory, anti-oxidant, and anti-apoptotic properties. However, the potential effects of EUG on T1DM had not been investigated. In this study, we established the streptozotocin (STZ)-induced T1DM mouse model in vivo and STZ-induced pancreatic {beta} cell MIN6 cell model in vitro to investigate the protective effects of EUG on T1DM, and tried to elucidate its potential mechanism. Our findings demonstrated that the intervention of EUG could effectively induce the activation of nuclear factor E2-related factor 2 (NRF2), leading to an up-regulation in the expressions of downstream proteins NQO-1 and HO-1, which are regulated by NRF2. Moreover, this intervention exhibited a significant amelioration in pancreatic {beta} cell damage associated with T1DM, accompanied by an elevation in insulin secretion and a reduction in the expression levels of apoptosis and oxidative stress related markers. Furthermore, ML385, an NRF2 inhibitor, reversed these effects of EUG. The present study suggested that EUG exerted protective effects on pancreatic {beta} cells in T1DM by attenuating apoptosis and oxidative stress through the activation of the NRF2 signaling pathway. Consequently, EUG holds great promise as a potential therapeutic candidate for T1DM.

pharmacology and toxicology↗

bioRxiv2024

Super Pangenome of Grapevines Empowers Improvement of the Oldest Domesticated Fruit

Grapevine (Vitis) is the oldest domesticated fruit crop with great cultural and economic importance. Here, we assemble and annotate haplotype-resolved genomes of 72 Vitis accessions including 25 wild and 47 cultivated grapevines, and a haplotype-resolved complete genome of V. vinifera. Coalescent phylogenomics of 142 haplotype genomes disentangles the mysterious hybridization history of grapevines, revealing enormous genetic diversity among species. Pangenome analysis together with phenotyping data reveals that European cultivars, more susceptible to the most destructive disease downy mildew (DM), had a smaller repertoire of disease resistance genes of NLR family. Through extensive structural variation (SV) characterization, phenotyping, transcriptome profiling of 113 Vitis accessions, and SV-eQTL analysis, we have identified over 79 SVs and their relevant genes significantly associated with DM resistance, exemplified by a lysine histidine transporter, VvLHT8. This haplotype-resolved complete genome and pangenome of Vitis genus will accelerate grapevine breeding and enrich our understanding of the evolution and biology of grapevines.

plant biology↗

bioRxiv2024

Sec23IP recruits the Cohen syndrome factor VPS13B/COH1 to ER exit site-Golgiinterface for tubular ERGIC formation

VPS13B/COH1 is the only known causative factor for Cohen syndrome, an early-onset autosomal recessive developmental disorder with intellectual inability, developmental delay, joint hypermobility, myopia and facial dysmorphism as common features, but the molecular basis of VPS13B/COH1 in pathogenesis is unknown. Here, we identify Sec23 interacting protein (Sec23IP) at ER exit site (ERES) as a VPS13B adaptor that recruits VPS13B to ERES-Golgi interfaces. VPS13B interacts directly with Sec23IP via the VPS13 adaptor binding domain (VAB), and the interaction promotes the association between ERES and the Golgi. Disease-associated missense mutations of VPS13B-VAB impair the interaction with Sec23IP. Knockout of VPS13B or Sec23IP blocks the formation of tubular ERGIC, an unconventional cargo carrier that expedites ER-to-Golgi transport. In addition, depletion of VPS13B or Sec23IP delays ER export of procollagen, suggesting a link between procollagen secretion and joint laxity in patients with Cohen disease. Together, our study reveals a crucial role of VPS13B-Sec23IP interaction at ERES-Golgi interface in the pathogenesis of Cohen syndrome.

cell biology↗

bioRxiv2023

Modern wheat breeding selection synergistically improves above- and below-ground traits

The root system, as a fundamental organ for uptaking water and nutrients and interacting with the local environmental conditions, has been postulated to be the foundation for a second Green Revolution. However, the status of the root system during modern wheat breeding remains to be elucidated. Here, by analyzing the phenotypes of 406 wheat accessions on a large scale, we found the root systems of modern cultivars were synchronisely changed along with the above-ground traits. Furthermore, the genomic blocks with phenotypic effects on both above- and below-ground traits were observed to be enriched in the selection sweeps, highlighting that modern wheat breeding contributed to the synchronised changes. More importantly, the haplotypes selected by breeders within the selection sweeps synergistically improved both the above- and below-ground traits, suggesting that modern wheat breeding has improved the root system indirectly, which may contribute to the higher grain yields of modern wheat cultivars. Our results demonstrated that modern wheat breeding synergistically improved the above- and below-ground traits.

genetics↗

bioRxiv2023

Dissecting peri-implantation development using cultured human embryos and embryo-like assembloids

Studies of cultured embryos have provided insights into human peri-implantation development. However, detailed knowledge of peri-implantation lineage developments as well as underlying mechanisms remain obscure. Using 3D-cultured human embryos, herein we report a complete cell atlas of the early post-implantation lineages and decipher cellular composition and gene signatures of the epiblast and hypoblast derivatives. In addition, we develop an embryo-like assembloid (E-assembloid) by assembling naive hESCs and extraembryonic cells. Using human embryos and E-assembloids, we reveal that WNT, BMP and Nodal signaling synergistically, but functionally differently, orchestrate human peri-implantation lineage development. Specially, we dissect mechanisms underlying extraembryonic mesoderm and extraembryonic endoderm specifications. Finally, an improved E-assembloid is developed to recapitulate the epiblast and hypoblast developments and tissue architectures in the pre-gastrulation human embryo. Our findings provide insights of the human peri-implantation development, and the E-assembloid offers a useful model to disentangle cellular behaviors and signaling interactions that drive human embryogenesis.

developmental biology↗

bioRxiv2023

Modeling and Simulation of Neocortical Micro- and Mesocircuitry. Part II: Physiology and Experimentation

Cortical dynamics underlie many cognitive processes and emerge from complex multi-scale interactions, which are challenging to study in vivo. Large-scale, biophysically detailed models offer a tool which can complement laboratory approaches. We present a model comprising eight somatosensory cortex subregions, 4.2 million morphological and electrically-detailed neurons, and 13.2 billion local and mid-range synapses. In silico tools enabled reproduction and extension of complex laboratory experiments under a single parameterization, providing strong validation. The model reproduced millisecond-precise stimulus-responses, stimulus-encoding under targeted optogenetic activation, and selective propagation of stimulus-evoked activity to downstream areas. The models direct correspondence with biology generated predictions about how multiscale organization shapes activity; for example, how cortical activity is shaped by high-dimensional connectivity motifs in local and mid-range connectivity, and spatial targeting rules by inhibitory subpopulations. The latter was facilitated using a rewired connectome which included specific targeting rules observed for different inhibitory neuron types in electron microscopy. The model also predicted the role of inhibitory interneuron types and different layers in stimulus encoding. Simulation tools and a large subvolume of the model are made available to enable further community-driven improvement, validation and investigation.

neuroscience↗

bioRxiv2023

Deciphering molecular heterogeneity and dynamics of neural stem cells in human hippocampal development, aging, and injury

While accumulated publications support the existence of neurogenesis in the adult human hippocampus, the homeostasis and developmental potentials of neural stem cells (NSCs) under different contexts remain unclear. Based on our generated single-nucleus atlas of the human hippocampus across neonatal, adult, aging and injury, we dissected the molecular heterogeneity and transcriptional dynamics of human hippocampal NSCs under different contexts. We further identified new specific neurogenic lineage markers that overcome the lack of specificity found in some well-known markers. Based on developmental trajectory and molecular signatures, we found that a subset of NSCs exhibit quiescent properties after birth, and most NSCs become deep quiescence during aging. Furthermore, certain deep quiescent NSCs are re-activated following stroke injury. Together, our findings provide valuable insights into the development, aging, and re-activation of the human hippocampal NSCs, and help to explain why adult hippocampal neurogenesis is infrequently observed in humans.

neuroscience↗

bioRxiv2023

MYPT1 is a non-canonical AKAP that tethers PKA to the MLCP signaling node

The activity of myosin light chain phosphatase (MLCP) is fine-tuned by the phosphorylation status of the MLCP target subunit 1 (MYPT1), which is determined by the antagonistic effects of Rho kinase (ROCK) and cAMP/cGMP-dependent protein kinases (PKA and PKG). PKA is composed of two regulatory (PKA-R, of which four variants exist) and two catalytic (PKAcat) subunits. PKA is targeted to the vicinity of its substrates by binding to A kinase anchoring proteins (AKAPs). MYPT1 is part of a complex signaling node that includes kinases and other enzymes involved in signal transduction. We hypothesized that MYPT1 might function as an AKAP to target PKA to the MLCP signaling node. Using a combination of immunoprecipitation, affinity pulldown and in situ proximity ligation assay (PLA) in human platelets and endothelial cells, we show that MYPT1 directly interacts with all four PKA-R variants and mapped the interaction to a 200 residues long central region of MYPT1. The interaction does not involve the docking and dimerization domain of PKA-R typically required for binding to AKAPs. Using peptide array overlay we identified K595, E676 and the PKA/ROCK kinase substrate motif R693/R694/S695/T696 as critical for the interaction. Substitution of S695, T696 or both by aspartic acid or the corresponding phosphorylated residue abolished binding. Our findings reveal that MYPT1 functions as a non-canonical AKAP to anchor PKA to the vicinity of non-phosphorylated S695/T696, where PKA-R would prevent PKAcat, and potentially also ROCK, from interacting with and phosphorylating MYPT1.

cell biology↗

bioRxiv2023

Dissecting embryonic and extra-embryonic lineage crosstalk with stem cell co-culture

Faithful embryogenesis requires precise coordination between embryonic and extraembryonic tissues. Although stem cells from embryonic and extraembryonic origins have been generated for several mammalian species(Bogliotti et al., 2018; Choi et al., 2019; Cui et al., 2019; Evans and Kaufman, 1981; Kunath et al., 2005; Li et al., 2008; Martin, 1981; Okae et al., 2018; Tanaka et al., 1998; Thomson et al., 1998; Vandevoort et al., 2007; Vilarino et al., 2020; Yu et al., 2021b; Zhong et al., 2018), they are grown in different culture conditions with diverse media composition, which makes it difficult to study cross-lineage communication. Here, by using the same culture condition that activates FGF, TGF-{beta} and WNT signaling pathways, we derived stable embryonic stem cells (ESCs), extraembryonic endoderm stem cells (XENs) and trophoblast stem cells (TSCs) from all three founding tissues of mouse and cynomolgus monkey blastocysts. This allowed us to establish embryonic and extraembryonic stem cell co-cultures to dissect lineage crosstalk during early mammalian development. Co-cultures of ESCs and XENs uncovered a conserved and previously unrecognized growth inhibition of pluripotent cells by extraembryonic endoderm cells, which is in part mediated through extracellular matrix signaling. Our study unveils a more universal state of stem cell self-renewal stabilized by activation, as opposed to inhibition, of developmental signaling pathways. The embryonic and extraembryonic stem cell co-culture strategy developed here will open new avenues for creating more faithful embryo models and developing more developmentally relevant differentiation protocols.

developmental biology↗

bioRxiv2022

Rewiring Cancer Drivers to Activate Apoptosis

Genes that drive the proliferation, survival, invasion and metastasis of malignant cells have been identified for many human cancers1-6. Independent studies have identified cell death pathways that eliminate cells for the good of the organism7-10. The coexistence of the cell death pathways with the driver mutations suggest that the cancer driver could be rewired to activate cell death. We have invented a new class of molecules: TCIPs (Transcriptional/Epigenetic Chemical Inducers of Proximity) that recruit the endogenous cancer driver, or a downstream transcription factor, to the promoters of cell death genes thereby activating their expression. To develop this concept, we have focused on diffuse large B cell lymphoma (DLBCL), in which BCL6 is amplified or mutated11. BCL6 binds to the promoters of cell death genes and epigenetically suppresses their expression12. We produced the first TCIPs by chemically linking BCL6 inhibitors to small molecules that bind transcriptional activators. Several of these molecules robustly kill DLBCL at single-digit nanomolar concentrations, including chemotherapy-resistant, TP53-mutant lines. The dominant gain-of-function approach provided by TCIPs captures the combinatorial specificity inherit to transcription and can thereby accesses new therapeutic space. TCIPs are relatively non-toxic to normal cells and mice, apparently reflecting their need for coincident expression of both target proteins for effective killing. The general TCIP concept has applications in elimination of senescent cells, enhancing expression of therapeutic genes, treatment of diseases produced by haploinsufficiency, and activation of immunogens for immunotherapy.

cancer biology↗

bioRxiv2022

A complex containing RhoBTB3-SHIP164-Vps26B promotes the biogenesis of early endosome buds at Golgi-endosome contacts

Early endosomes (EEs) are central hubs for cargo sorting in vesicular trafficking. Cargoes destined for degradation retain in EEs that are eventually delivered to lysosomes, while recycled cargo destined for the plasma membrane (PM) or to the Golgi are segregated into EE buds, a specialized membrane structure transiently generated on EEs during cargo sorting. Until now, the molecular basis of the membrane expansion during the biogenesis of EE buds is completely elusive. Here, we identify a protein complex containing a Vps13 domain-containing lipid transporter SHIP164, ATPase RhoBTB3 and retromer component Vps26B, promotes the membrane expansion in the biogenesis of EE buds at Golgi-EE contacts. SHIP164 depletion specifically reduces the size and number of EE buds marked by Vps26B and actin, and results in less but enlarged EEs, which can be substantially rescued by wild type SHIP164 other than lipid transfer-defective mutants, suggesting a role of lipid transfer of SHIP164 in the process. SHIP164 and RhoBTB3 interact with enzymes for phospholipid synthesis on motile Golgi vesicles, that frequently contact EEs. Functionally, SHIP164 depletion substantially reduces the trafficking of sphingomyelin to the PM, and impairs cell growth. Together, we propose a lipid transport-dependent route from the Golgi to EEs at the contacts required for EE bud biogenesis.

cell biology↗

bioRxiv2022

Multi-environmental population phenotyping suggest the higher risks of wheat Rht-B1b and Rht-D1b cultivars in global warming scenarios

After six decades practice, the semi-dwarf alleles Rht-B1b and Rht-D1b (also called Rht-1 and Rht-2) had been applied into around 70% current wheat cultivars, laid the foundation for the worldwide wheat production supply, then the agronomic traits controlled by the two alleles still keep unclear except dwarfing wheat. Here 13 agronomic traits were investigated in 400 wheat accessions with seven environments, uncovered the genetic effects of Rht-B1b and Rht-D1b on wheat structure and yield traits in different genetic backgrounds and environments, and the distinct genetic effects between Rht-B1b and Rht-D1b, suggesting that the introduction of green revolution alleles profoundly shaped the agronomy traits of modern wheat cultivars. The late-sowing assays and regression analysis based on the phenotypic and their meteorological data showed the accessions containing Rht-B1b and Rht-D1b are more sensitive to the temperature increase, and the Rht-D1b may lost additional 8% yield compared the cultivars without the green revolution alleles if the average temperature increases 1 {degrees}C. These results suggest the application of green revolution are facing more challenges to maintain the futural wheat production supply in global warming scenarios.

molecular biology↗

bioRxiv2022

Specialized metabolism by trichome-preferentially-expressed Rubisco and fatty acid synthase components

Acylsugars, specialized metabolites with defense activities, are secreted by trichomes of many solanaceous plants. Several acylsugar metabolic genes (AMGs) remain unknown. We previously reported multiple candidate AMGs. Here, using multiple approaches, we characterized additional AMGs. First, we identified differentially expressed genes between high- and low-acylsugar-producing F2 plants derived from a cross between Solanum lycopersicum and S. pennellii, which produce acylsugars [~]1% and [~]20% of leaf dry weight, respectively. Expression levels of many known and candidate AMGs positively correlated with acylsugar amounts in F2 individuals. Next, we identified lycopersicum-pennellii putative orthologs with higher nonsynonymous to synonymous substitutions. These analyses identified four candidate genes, three of which showed enriched expression in stem trichomes compared to underlying tissues (shaved stems). Virus-induced gene silencing confirmed two candidates, Sopen05g009610 [beta-ketoacyl-(acyl-carrier-protein) reductase; fatty acid synthase component] and Sopen07g006810 (Rubisco small subunit), as AMGs. Phylogenetic analysis indicated that Sopen05g009610 is distinct from specialized metabolic cytosolic reductases, but closely related to two capsaicinoid biosynthetic reductases, suggesting evolutionary relationship between acylsugar and capsaicinoid biosynthesis. Additionally, data mining revealed that orthologs of Sopen05g009610 are preferentially expressed in trichomes of several acylsugar-producing solanaceous species. Similarly, orthologs of Sopen07g006810 were identified as trichome-preferentially-expressed members, which form a phylogenetic clade distinct from those of mesophyll-expressed "regular" Rubisco small subunits. Furthermore, {delta}13C analyses indicated recycling of metabolic CO2 into acylsugars by Sopen07g006810 and shed light on how trichomes support high levels of specialized metabolite production. These findings have implications for genetic manipulation of trichome specialized metabolism in solanaceous crops, including tomato, potato, and tobacco.

plant biology↗