Biology subjects

Cheng, T.

Publications and source records attributed to Cheng, T..

At least 19 recordsLinked to original sources

bioRxiv2026

Substrate biasing in UCHL5 proteoforms

Proteolytic deubiquitinating enzymes bridge a gap in substrate recognition through complex regulatory mechanisms. A growing portion of these are accomplished through proteoforms that uniquely control association and diverse sets of cleavage capabilities that relay distinct physiological outcomes. This study describes substrate biasing governed by UCHL5 proteoforms. It demonstrates that N-terminal ubiquitination activates the enzyme towards monoubiquitin substrates, a feature that is conserved across UCHL5 homologs. Crystallographic and spectroscopic data suggest that the N-terminal ubiquitin binds intramolecularly in an allosteric binding site and inhibits branched chain substrate cleavage. Association with Rpn13/Adrm1 relieves this inhibition and reestablishes its ability to debranch, potentially controlling nonspecific debranching compared to retention of needed activity on the 26S proteasome. Collectively, this study describes the molecular basis for substrate selectivity in a deubiquitinating enzyme, an unexplored area in the enzymes that counteract ubiquitin E3 ligases.

biochemistry↗

bioRxiv2026

Microbiota-derived TMAO links PM2.5 exposure to cognitive impairment: A gut liver brain axis

Although fine particulate matter (PM2.5) is linked to cognitive impairment, the mechanistic links between pulmonary exposure and neurodegeneration remain poorly understood. This study investigates the role of the gut-liver-brain axis in mediating PM2.5-induced neurotoxicity. We demonstrate that three weeks of intratracheal PM2.5 instillation in mice causes significant memory deficits, impaired hippocampal adult neurogenesis, and reduced synaptic plasticity in both sexes. Metagenomic analysis revealed that PM2.5 alters gut microbiota composition, specifically by upregulating pathways involved in trimethylamine (TMA) synthesis. This microbial shift led to a systemic increase in the metabolite trimethylamine N-oxide (TMAO) and its accumulation in the hippocampus. Mechanistic experiments revealed that TMAO drives neurotoxicity by activating the hippocampal PERK-mediated endoplasmic reticulum (ER) stress pathway. Critically, these deficits were reversed by suppressing hepatic TMAO production via either pharmacological inhibitors or genetic knockdown. Additionally, hippocampal-specific PERK silencing or dietary resveratrol intervention attenuated hippocampal ER stress, thereby protecting against PM2.5-induced cognitive and hippocampal impairments. These results identify the microbial metabolite TMAO as a key mediator of air pollution-related neurotoxicity and highlight the gut-liver-brain axis as a promising therapeutic strategy to counteract the neurological impacts of air pollution.

animal behavior and cognition↗

bioRxiv2026

Calcium-dependent synaptic proteomics reveals EGFR signaling at active synapses

Activity-dependent remodeling of the synaptic proteome is essential for circuit maturation, plasticity, and adaptation. However, these molecular changes are transient and spatially sparse in intact neural circuits, making them difficult to resolve under physiological conditions. To address this challenge, we developed synaptic Cal-ID, a synapse-targeted, calcium-dependent proximity labeling strategy that enables activity-resolved proteomic profiling under native physiological conditions. Using synaptic Cal-ID, we uncover an unexpected mechanism by which synaptic activity locally engages epidermal growth factor receptor (EGFR) signaling. We identify two novel synaptic proteins, Anks1a and Ubash3b, that are rapidly recruited following activity and cooperatively promote postsynaptic enrichment and signaling of EGFR. Disruption of this pathway impairs synaptic maturation, plasticity, and memory. Together, these findings reveal how neuronal activity establishes local signaling competence at active synapses by concentrating the molecular machinery required to engage a broadly acting growth factor pathway.

neuroscience↗

bioRxiv2026

Biohybrid Robots with Embedded Conductive Fibers for Actuation, Sensing, and Closed-loop Control

Living organisms achieve adaptive actuation through the seamless integration of neural motor control circuitry and proprioceptive feedback. While biohybrid robotics aims to replicate these capabilities by merging engineered muscle with synthetic scaffolds, the field remains limited by interfaces that lack the efficiency and closed-loop regulation of natural neuromuscular systems. Here, we introduce a biohybrid muscle actuator system featuring a bioelectronic interface based on soft poly(3,4-ethylenedioxythiophene) (PEDOT) fibers for stimulation and sensing. These fibers conformally couple to muscle tissues, eliciting robust contractions at voltages as low as 1 V--requiring ultra-low power (0.376 {+/-} 0.034 mW) and preserving long-term tissue viability. By leveraging the independent addressability of these fibers, we demonstrate selective actuation of individual muscle units to achieve precise spatiotemporal control of a two-muscle-powered walking biohybrid robot, reaching a locomotion speed of 5.43 {+/-} 0.79 mm/min. When configured as strain sensors, the fibers exhibit a high gauge factor of 155.45 {+/-} 6.59 and resolve contractile displacements within tens of micrometers. We demonstrate that this sensing modality can be integrated into a closed-loop controller to autonomously modulate stimulation based on real-time feedback, significantly mitigating muscle fatigue (p = 0.038) during continuous operation. This work establishes a versatile platform for efficient actuation and intrinsic feedback sensing, providing a blueprint for efficient, autonomous, and adaptive biohybrid machines. SummarySoft conductive fibers enable a bioelectronic interface for low-power actuation and closed-loop control in biohybrid robots.

bioengineering↗

bioRxiv2026

Protocol-dependent cardiomyocyte states determine disease modelling capacity of human iPSCs

Human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) are widely used to model cardiovascular disease, yet numerous differentiation protocols generate cardiomyocytes with heterogeneous molecular and functional properties, complicating experimental design. Here we systematically compare sixteen commonly used cardiomyocyte differentiation protocols and characterize their resulting cell states using single-nucleus RNA sequencing, functional phenotyping and computational integration with human genetic data. Despite similar cardiomyocyte yields, protocols produced distinct transcriptional programs, subtype compositions and physiological properties. By integrating protocol-specific gene expression signatures with genome-wide association studies of cardiovascular traits, we identify cardiomyocyte states enriched for genetic architectures underlying specific diseases. These analyses accurately predict protocols most suitable for modelling particular disease contexts, including electrophysiological defects associated with Brugada syndrome and metabolic vulnerability relevant to myocardial infarction. Our results demonstrate that differentiation protocols encode biologically distinct cardiomyocyte states with differential disease relevance and establish a framework for aligning stem-cell differentiation strategies with human complex trait genetics to guide model selection. This approach enables rational design of iPSC-based disease models and highlights how population-scale genetic data can inform experimental systems in stem cell biology.

systems biology↗

bioRxiv2026

Morphological transformation in Helicobacter pylori is a dynamic process leading to two types of coccoid

The helical shape of Helicobacter pylori is crucial for successful colonization of the human stomach. However, this pathogen can shapeshift into another form termed the "coccoid form" with a spherical shape, through a mechanism that remains elusive. Here, by a combination of fluorescence microscopy using fluorescent D-aminoacids, cryoelectron and atom force microscopy, we explored the dynamics of coccoid formation in H. pylori through interrogation of the peptidoglycan layer. Contrary to the widely held hypothesis, we showed that helical-rod H. pylori transformed into a coccoid without transiting through a U-form. We show that U-forms, characterized by a U-shaped peptidoglycan with enlarged periplasmic space, altered genetic material, and red autofluorescence, are the output of a parallel pathway, which, unlike the coccoid pathway, is independent of the HdpA/Csd3 peptidoglycan endopeptidase. Coccoid formation occurred along a rigid timeline, by bulging of the cytoplasmic membrane through a peptidoglycan crack, resulting in a spheroplast-like structure with the peptidoglycan stacked into a thick layer near the original cell poles. Resistance of that structure against lysis likely involves a switch in metabolic profile reminiscent of bacteria in dormancy, with a notable accumulation of lysophospholipids, demonstrated in this work. Altogether, the ultrastructure and properties of H. pylori coccoids evidenced here are compatible with a role of this form in relapse after antibiotic treatment. SIGNIFICANCE STATEMENTUpon prolonged growth, stomach pathogen Helicobacter pylori undergoes a morphological change from a helical to a spherical form called coccoid, which may be involved in bacterial persistence and immune evasion. The pathway leading to this form, as well as its precise architecture, were unclear. In this work, we show by different microscopy techniques that the transition to coccoid does not involve a U-shaped intermediate as proposed before, but is triggered by progressive thinning, due to the activity of endopeptidase HdpA/Csd3, of the peptidoglycan meshwork that normally protects the cell, eventually leading to rupture. Because of the hole thus created, peptidoglycan can no longer contain the osmotic pressure in the cytoplasm, which leaks out within a membrane bulge, to eventually give rise to a kind of sphaeroplast, expected to be insensitive to cell wall-targeted antibiotics.

microbiology↗

bioRxiv2025

Identification of molecular and clinical ALS subgroups based on TDP-43 loss of function molecular markers from population-based patient-derived iPS motor neurons

BackgroundAmyotrophic lateral sclerosis (ALS) is a uniformly fatal neurodegenerative disease characterized by progressive cortical and spinal motor neuron loss, with most patients surviving only 2-5 years post-diagnosis. While approximately 10% of cases are familial (fALS), the remaining 90% are sporadic (sALS) with unknown genetic drivers. Importantly, clinical presentations are heterogeneous in both sporadic and familial ALS, underscoring the complexity of the disease. A pathological hallmark of ALS is the mislocalization of RNA-binding protein TDP-43 from the nucleus to the cytoplasm. This mislocalization produces both loss of function consequences, such as widespread RNA processing and splicing defects, as well as potential toxic gain of function effects associated with cytoplasmic aggregation. ResultsIn this study, we used RT-PCR data from induced pluripotent stem cell-derived motor neurons derived from 180 sALS and C9orf72 fALS patients from the Answer ALS collection to identify biological subgroups based on TDP-43 loss-of-function signatures. Spectral embedding revealed four distinct molecular clusters, including one subgroup genetically similar to controls and another with the most dysregulated mRNA expression, suggesting differing disease severity. Linear mixed models were then used to assess the longitudinal trajectory of over 90 clinical measures, and the between-cluster interaction effects were evaluated. Conclusions36 clinical outcomes showed significant differences across clusters, supporting the presence of biologically and clinically distinct ALS subtypes based on the TDP-43 associated pathogenic cascade. These findings demonstrate a critical role of RNA profiling in uncovering biologically meaningful subtypes of ALS, potentially allowing for more precise prognostic tools and the development of future personalized therapeutic approaches.

neuroscience↗

bioRxiv2025

Structural and Functional Insights into HBx-Smc6 Targeting for HBV Inhibition

The hepatitis B virus (HBV) X protein (HBx) is a multifunctional regulator essential for HBV replication and HBV-associated hepatocarcinogenesis. Despite its central role, the molecular basis of HBx function has remained elusive. Here, we present the first cryo-electron microscopy structure of the human HBx-CRL4-Smc5/6 complex at 3.1 [A] resolution. In this reconstituted ten-subunit assembly, HBx adopts a Zn2 {square}-stabilized Y-shaped architecture that simultaneously engages the DDB1 and the Smc6 subunit. A composite helix-turn-helix (HTH) pocket in HBx accommodates a conserved "Leucine Key" motif (LRCKL) on Smc6, forming a critical interface essential for complex stability and function. Molecular docking and biochemical validation reveal that the compound Tranilast binds this HTH pocket, disrupts the HBx-Smc6 interaction, and suppresses HBV replication. These findings define the structural mechanism by which HBx counteracts host restriction and establish the HBx-Smc6 interface as a previously unrecognized and druggable target for antiviral intervention.

cell biology↗

bioRxiv2025

Architecture of a peptidoglycan peptidase complex involved in morphological transition in Helicobacter pylori.

Peptidoglycan is a meshwork macromolecule, made of polysaccharide strands cross-linked by short peptides, which encases the cytoplasmic membrane of bacteria and protects them against turgor pressure. Peptidoglycan peptidases are membrane or periplasmic enzymes that cleave these peptides, either lowering the cross-linking level of peptidoglycan to sculpt bacterial shape or allowing cell elongation by making space for the insertion of neosynthesized glycan strands. In the pathogen Helicobacter pylori, shape is important for virulence, and transition to a coccoid form after prolonged growth enables immune evasion. One particular endopeptidase, HdpA, is known to be involved in the maintenance of cell shape and in the transition to coccoids. Here we show that along growth, HdpA is constantly associated with LhiA, an inner membrane chaperone lipoprotein that keeps it in check while protecting it from fast proteolysis. The crystal structure of the HdpA-LhiA complex suggests that this interaction freezes the autoinhibitory interaction between the first domain of HdpA and the third, catalytic domain. Analysis of the evolution of the HdpA and LhiA protein levels over growth suggests that transition to coccoids is not triggered by a burst in HdpA activity but rather by a gradual weakening of the sacculus caused by the small fraction of free HdpA in equilibrium with LhiA-sequestered HdpA. SIGNIFICANCE STATEMENTThe cell wall, the exoskeleton of bacteria, is the target of numerous antibiotics. Its principal component, peptidoglycan, is remodeled by an interplay between peptidoglycan synthases and hydrolases to accomodate bacterial growth. Because their activity can be harmful, hydrolases have to be tightly regulated. We discovered the dedicated inhibitory chaperone of a H. pylori peptidoglycan hydrolase and showed how the chaperone keeps the hydrolase in check in the cytoplasmic membrane and releases it slowly to allow it to perform its task, ultimately triggering a shape transition to a spherical form important for immune evasion. The crystal structure of the complex gives clues to the mechanism of peptidase activation, suggesting strategies to design agonists that could be used as antibacterials.

microbiology↗

bioRxiv2025

Angptl5 restricts primitive hematopoiesis by modulating retinoic acid signaling in zebrafish

Homeostasis is essential for hematopoiesis, and its dysregulation can lead to severe pathological conditions. Retinoic acid (RA) is a key regulator that exerts concentration-dependent effects on both embryonic and adult hematopoiesis. However, the mechanisms that modulate RA signaling in hematopoietic processes remain poorly understood. Using zebrafish as a model, we identified angiopoietin-like protein 5 (Angptl5) as a critical regulator of hematopoietic homeostasis. Loss of Angptl5 function resulted in myeloid hyperplasia in the anterior lateral plate mesoderm (ALPM) and anterior expansion of erythroid progenitors in the posterior lateral plate mesoderm (PLPM)-- phenotypes consistent with attenuated RA signaling. Molecular analyses confirmed impaired RA signaling in angptl5{Delta}10/{Delta}10 mutants, and exogenous RA supplementation fully rescued the hematopoietic defects. Mechanistically, we found that Angptl5 transcriptionally activates retinol dehydrogenase dhrs9 through its interaction with Integrin 6l{beta}5. Our findings establish Angptl5 as a novel and essential regulator of embryonic hematopoiesis and reveal a previously unrecognized mechanism controlling hematopoietic homeostasis. These insights position Angptl5 as a potential therapeutic target for hematological disorders.

developmental biology↗

bioRxiv2025

Tree bark as a substrate for mycelium-bound composites with two Ganoderma species

Bark is currently considered as a by-product of the wood industry and is mostly incinerated for energy, left in forests, or used as a mulch layer in gardens, parks, and forests to help prevent soil from drying out. However, considering that bark makes up about 10-20% of the tree volume, there is a considerable amount of material that can be exploited and should be investigated in terms of a resource-efficient bio-economy. One way to use bark as a raw material for innovative products could be as a substrate within mycelium-bound composite materials. However, since one of the natural functions of bark is to inhibit microbial infestation of the trees, it was unclear whether bark could be utilized in this manner. Therefore, we investigate in this study the possibilities of producing such composites by evaluating the performance of several bark-fungus combinations. Three different barks (from Douglas fir, Scots pine and European birch) and two species of fungi (Ganoderma sessile and Ganoderma adspersum) were selected for the experiments. Mycelium growth rates were evaluated with a newly developed method using fungal "growth tubes". In addition, composites were prepared for performance tests from pure bark and 1:1 mixtures of bark and beech wood sawdust. Composites made of mixed bark and beech wood were mostly well overgrown with a thick layer of mycelium on the surface, supporting higher compression strengths. The mycelium layer on the composites made with tree bark only was considerably thinner, resulting in lower compression strength. Water absorption potential was found to be highly dependent on the mycelium layer on the composite surfaces, which has substantial hydrophobic properties. Overall, although the required incubation times tend to be longer than for other commonly used substrates, our experiments demonstrate that bark clearly represents a potential co-substrate for the production of mycelium-bound composites. Nevertheless, further studies with different fungi and barks are required to identify mixtures for specific applications that require shorter incubation times.

bioengineering↗

bioRxiv2024

BMP4 is sufficient to induce a caudal organizer

The caudal part of a vertebrate embryo consists of somites, neural tube, lateral plate mesoderm derivatives and the tailbud. However, the minimal conditions and factors sufficient to induce the caudal region, particularly in humans, remain unresolved. Here, we show that BMP4 alone, when administered at appropriate dosage, is sufficient to induce the formation of an organizer for caudal induction. This organizer induces caudal cell fate specification and morphogenesis in zebrafish embryos. In 3D human pluripotent stem cells (hPSCs) aggregates, BMP4 can induce an elongated embryonic structure characterized by caudal fates. Importantly, hPSCs instructed by BMP4 are sufficient to induce a secondary caudal region when grafted into the animal pole of the zebrafish embryo. Our study thus uncovers BMP4 as the inducer in the formation of a caudal organizer in the vertebrate embryo. Significance statementWe demonstrate that BMP4 alone can induce the formation of a caudal organizer, a critical structure that guides the development of the caudal region in vertebrates. Using zebrafish embryos, embryonic explants, human pluripotent stem cell xenografts, and 3D human stem cell aggregates, we show that this organizer replicates morphogenesis and key differentiation pathways seen in natural development. Our findings uncover a novel role for BMP4 and define the minimal requirements for inducing this organizer, offering new insights into vertebrate development and potential applications in regenerative medicine.

developmental biology↗

bioRxiv2024

Mycn regulates vascular development through PI3K signaling pathway in zebrafish

Mycn, a MYC gene family member, is implicated in both carcinogenesis through amplification and Feingold syndrome through its deficiency. Previous studies have indicated that increased Mycn expression enhances vascularization in human neuroblastomas, yet its precise role in vascular development remains elusive. In this study, we utilized single-cell RNA-seq and live imaging analyses to confirm that mycn is expressed during zebrafish vasculogenesis. We investigated vascular development in zebrafish using a genetically engineered mycn mutation. Our findings reveal that mycn-deficient zebrafish exhibit reduced intersegmental vessels and malformed subintestinal vessels, primarily due to decreased cell proliferation in vascular cells. Importantly, we discovered that activation of PI3K signaling significantly ameliorates these vascular abnormalities.

developmental biology↗

bioRxiv2024

Deciphering tumour microenvironment and elucidating the origin of cancer cells in ovarian clear cell carcinoma

Ovarian clear cell carcinoma (CCC) has an East Asian preponderance. It is associated with endometriosis, a benign condition where endometrial (inner lining of the uterus) tissue is found outside the uterus and on the peritoneal surface, in the abdominal or pelvic space. CCC is relatively more resistant to conventional chemotherapy compared to other ovarian cancer subtypes and is associated with a poorer prognosis. In this study, we recruited and obtained tumour tissues from seven patients across the four stages of CCC. The tumour and the tumour microenvironment (TME) from 7 CCC patients spanning clinical stages 1-4 were transcriptionally profiled using high-resolution scRNA-seq to gain insight into CCCs biological mechanisms. Firstly, we built a scRNA-seq resource for the CCC tumour microenvironment (TME). Secondly, we identified the different cell type proportions and found high levels of immune infiltration in CCC. Thirdly, since CCC is associated with endometriosis, we compared CCC with two publicly available endometriosis scRNA-seq datasets. The CCC malignant cells showed similarities with glandular secretory and ciliated epithelial cells found in endometriosis. Finally, we determined the differences in cell-cell communication between various cell types present in CCC TME and endometriosis conditions to gain insights into the transformations in CCC.

cancer biology↗

bioRxiv2024

Unravelling the progression of the zebrafish primary body axis with reconstructed spatiotemporal transcriptomics

Elucidating the spatiotemporal dynamics of gene expression is essential for understanding complex physiological and pathological processes. Traditional technologies like in situ hybridization (ISH) and immunostaining have been restricted to analyzing expression patterns of a limited number of genes. Spatial transcriptomics (ST) has emerged as a robust alternative, enabling the investigation of spatial patterns of thousands of genes simultaneously. However, current ST methods are hindered by low read depths and limited gene detection capabilities. Here, we introduce Palette, a pipeline that infers detailed spatial gene expression patterns from bulk RNA-seq data, utilizing existing ST data as only reference. This method identifies more precise expression patterns by smoothing, imputing and adjusting gene expressions. We applied Palette to construct the Danio rerio SpatioTemporal Expression Profiles (DreSTEP) by integrating 53-slice serial bulk RNA-seq data from three developmental stages with existing ST references and 3D zebrafish embryo images. DreSTEP provides a comprehensive cartographic resource for examining gene expression and spatial cell-cell interactions within zebrafish embryos. Utilizing machine learning-based screening, we identified key morphogens and transcription factors (TFs) essential for anteroposterior (AP) axis development and characterized their dynamic distribution throughout embryogenesis. In addition, among these TFs, Hox family genes were found to be pivotal in AP axis refinement. Their expression was closely correlated with cellular AP identities, and hoxb genes may act as central regulators in this process.

developmental biology↗

bioRxiv2024

Multi-omics profiling of mouse polycystic kidney disease progression at a single cell resolution

Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease and causes significant morbidity, ultimately leading to end-stage kidney disease. PKD pathogenesis is characterized by complex and dynamic alterations in multiple cell types during disease progression, hampering a deeper understanding of disease mechanism and the development of therapeutic approaches. Here, we generate a single nucleus multimodal atlas of an orthologous mouse PKD model at early, mid and late timepoints, consisting of 125,434 single-nucleus transcriptomic and epigenetic multiomes. We catalogue differentially expressed genes and activated epigenetic regions in each cell type during PKD progression, characterizing cell-type-specific responses to Pkd1 deletion. We describe heterogeneous, atypical collecting duct cells as well as proximal tubular cells that constitute cyst epithelia in PKD. The transcriptional regulation of the cyst lining cell marker GPRC5A is conserved between mouse and human PKD cystic epithelia, suggesting shared gene regulatory pathways. Our single nucleus multiomic analysis of mouse PKD provides a foundation to understand the earliest changes molecular deregulation in a mouse model of PKD at a single-cell resolution.

genomics↗

bioRxiv2024

Calneuron 1 reveals the pivotal roles in schizophrenia via perturbing human forebrain development and causing hallucination-like behavior in mice

Schizophrenia is a highly heritable neurodevelopmental disorder with unknown genetic pathogenic mechanisms. Here, we selected 11 schizophrenia risk genes and generated single-gene-knockout-precise-dorsal/ventral-forebrain-organoids (SKOPOS) via CRISPR-Cas9 system. 90 bulk and 249,430 single-cell RNA-sequencing of SKOPOS revealed that knockout of 11 risk genes lead to different levels of deficits in dorsal/ventral forebrain organoids. Among them, calneuron 1 (CALN1) acts as a pivotal pathogenic gene of schizophrenia via severe disruption of gene expression network, interaction with about 32% (34/106) known schizophrenia risk genes, delayed maturation and impaired spontaneous neural circuit in human developing forebrain. Furtherly, including the spontaneous abrupt burst spiking in cortical neurons and the defects of spatial memory, cognition and social ability, Caln1 KO mice surprisingly displayed spontaneous startle behavior and head-twitch response correlated with hallucination-like behavior, which could be inhibited by antipsychotic drug SEP-363856. In summary, CALN1 is identified as a pivotal pathogenic gene of schizophrenia in forebrain development.

neuroscience↗

bioRxiv2024

Development of a Two-Leaf Photosynthetic Model Sensitive to Chlorophyll and Its Coupling with a Wheat Growth Model

Crop growth models (CGMs) commonly simulates the response of photosynthetic rate to nitrogen (N) dynamic by calculating critical N concentration. However, critical N concentration makes it hard to describe the physiological effect of N dynamic on photosynthesis. Meanwhile, the effect of diffuse light on photosynthesis was limited in previous studies. In this study, we introduced a Two-leaf Photosynthetic Model Sensitive to Chlorophyll Content (TPMSCC) and coupled it with the crop growth model (WheatGrow) to enhance our understanding of how N dynamic and diffuse light affects photosynthesis. By coupling the Farquhar-von Caemmerer-Berry (FvCB) C3 photosynthesis model with a canopy radiative transfer model (PROSAIL), TPMSCC simulated the light interception of direct and diffuse light, and employed leaf chlorophyll content (LCC) to simulate the light absorption and electron transfer rate of leaves. Result showed that TPMSCC well simulated the light absorption of the wheat canopy and found the canopy photosynthetic rate benefited from the increase of diffuse radiation fraction (DRF) except for when the condition of a dense canopy at a high solar zenith angle was present. Research found the logarithmic and linear relationships of LCC to the initial light use efficiency ([a]) and the maximum photosynthetic rate (Amax), respectively, which followed the field measurements. Additionally, the optimized WheatGrow model outperforms its predecessor in describing the response of N application rate on photosynthesis.

biophysics↗