Biology subjects

Shen, C.

Publications and source records attributed to Shen, C..

At least 37 records · Page 2Linked to original sources

bioRxiv2025

Intrinsic structure of lipoplexes embedded in polyelectrolyte multilayers

The functionalization of surfaces with therapeutically applicable nucleic acid carriers provides promising strategies in biomedical research to develop therapies which focus on local nucleic acid delivery. One such approach is the embedding of lipoplexes (LPXs) in polysaccharide-based polyelectrolyte multilayers (PEMs). PEMs based on hyaluronic acid and chitosan lead to efficient embedding of customized LPX connected with good biological activity. However, although quantitative evaluation demonstrates LPX embedding, information on the embedded LPXs has been missing. In this study we used synchrotron-based grazing-incidence small angle x-ray scattering to investigate the effects of the change in the chemical environment caused by the embedding into PEMs on the LPXs internal mesoscopic structure. While the lamellar character of the LPXs was preserved, the repeat distance was affected by the embedding into polysaccharide-based coatings.

biophysics↗

bioRxiv2025

TIPP-SD: A New Method for Species Detection in Microbiomes

In this study, we present TIPP-SD (i.e., TIPP for Species Detection), a new technique for species detection in a microbiome sample. TIPP-SD uses a modified version of TIPP3, which is a recently developed abundance profiling tool based on maximum likelihood phylogenetic placement into marker gene taxonomies. TIPP-SD depends on a parameter (i.e., "thresh-old") for the required support for species detection, thus allowing us to compute a precision-recall curve as we vary this parameter. In comparing the precision-recall curves for TIPP-SD, TIPP3, Kraken2, Bracken, and Metapresence, we find that TIPP-SD improves on the other methods with respect to accuracy under conditions where some species occur in low abundance, or where there is sequencing error. Under easier conditions, TIPP-SD is close to the best of these methods. Finally, although TIPP-SD is slower than Kraken2 and Bracken, it is still fast enough to be used on large datasets.

bioinformatics↗

bioRxiv2025

Photochemical modification of two fluorene-based molecules yields structurally distinct DNA intercalators with potent anti-MRSA activity

Staphylococcus aureus is a leading cause of skin and soft tissue infections, endocarditis, and bloodstream infections worldwide. The emergence of methicillin-resistant S. aureus (MRSA) and growing resistance to last-resort antibiotics like vancomycin have created an urgent need for new antimicrobials with distinct mechanisms of action. In this study, we characterize DB10, a planar, fluorene-based compound identified in a high-throughput screen for MRSA inhibitors. Upon UVA exposure, DB10 undergoes photoconversion from a red-colored form (DB10-R) to a yellow-colored form (DB10-Y). In comparison with DB10-R, DB10-Y exhibits reduced hydrophobicity, lower cytotoxicity, and modestly improved minimum inhibitory concentrations (MICs) towards a number of Gram-positive bacteria. DB10-Y intercalates into DNA and induces double-stranded breaks, yet resistance emerged only at low levels after prolonged serial passaging. To optimize this scaffold, we screened a panel of fluorene analogs and identified the photoconverting analog DB33, which in its yellow form (DB33-Y) is non-toxic and retained DNA intercalation activity. DB33-Y was effective against intracellular S. aureus in macrophages and epithelial cells and significantly reduced bacterial burden and lesion size in a murine skin infection model. DB10-Y and DB33-Y both also suppressed expression of -toxin at sub-MIC concentrations, indicating an additional anti-virulence effect. Together, these findings highlight the therapeutic potential of fluorene-based DNA intercalators as a new class of antimicrobial and anti-virulence agents against MRSA.

microbiology↗

bioRxiv2025

Lipid monolayers adsorbing mRNA as models for mRNA enclosed in lipid nanoparticles for transfection

In lipid-based mRNA pharmaceuticals applicable for vaccination, cancer therapy, and other types of therapeutics, the negatively charged RNA is embedded in nanoparticles containing positively charged or ionizable lipids. The local cohesion at the lipid-RNA interface plays an important role for the stability and biological activity of the resulting nanoparticles. Ions and other buffer components in the RNAs immediate surroundings may affect RNA stability against hydrolysis and its binding strength to the oppositely charged lipid layers, which is relevant for release after cellular uptake and endosomal processing. Here, we use Langmuir monolayers at the air/water interface as well-defined experimental models to study the local molecular organization of mRNA adsorbed to lipid layers. Binding of mRNA in the presence of monovalent and divalent ions from the aqueous phase to monolayers consisting of cationic transfection lipids and zwitterionic phospholipids is investigated with synchrotron-based x-ray fluorescence and scattering techniques. The experiments provide detailed insights into the structure of the adsorbed layers as well as the fractions of all molecular moieties contributing to the interfacial electrostatic balance, specifically phosphates from RNA, phosphates from phospholipids in the monolayer, and elemental counterions. The mRNA forms discrete electron-dense layers tightly bound to the lipid membrane, where cationic ions accumulate at the interface together with the mRNA. This leads to an excess of anionic nucleotides relative to cationic lipids at the interface, which is more pronounced in the presence of divalent compared to monovalent cations. The quantitative information on local interfacial moieties obtained here may constitute a valuable basis for the evaluation of quality aspects of nanoparticles comprising mRNA in the bulk phase.

biophysics↗

bioRxiv2025

HSF4: A Prognostic Predictor and Potential Therapeutic Target in Colorectal Cancer with Implications for Patient Immune Status

Colorectal cancer (CRC) is among the most prevalent malignancies globally, characterized by high morbidity and mortality rates. The Heat Shock Factor (HSF) family of genes plays a critical role in the cellular response to environmental stress, particularly heat stress. These genes encode transcription factors that regulate the expression of heat shock proteins, which are essential for maintaining cellular homeostasis under stressful conditions. Recently, there has been a growing interest in the role of HSF family genes in the development and progression of CRC. In this study, we conducted a comprehensive analysis of CRC samples from The Cancer Genome Atlas (TCGA) database to identify potential therapeutic targets. A total of 533 gene expression matrices, were downloaded and processed, including 42 normal and 491 tumor samples. Differential expression analysis of the HSF family genes, revealed HSF4 as the most significantly differentially expressed gene between normal and tumor samples. Consequently an HSF4-related signature was constructed, stratifying all CRC patients in the TCGA dataset into low-risk or high-risk groups based on HSF4 expression. Survival analysis demonstrated a significant association between HSF4 expression and clinical outcomes indicating that the signature possesses substantial. Correlation analysis further revealed significant relationships between HSF4 expression and clinical features including Stage, T stage, M stage, and N stage. Univariate and multivariate Cox regression analyses confirmed the prognostic significance of HSF4. Functional analysis of differentially expressed genes based on HSF4 expression levels demonstrated enrichment in critical biological processes and pathways. Furthermore, HSF4 exhibited unique properties within the tumor microenvironment (TME). Additional analysis indicated that different risk groups exhibit varying levels of immune cell infiltration and cell proliferation capacity. Notably, the low-risk group showed increased sensitivity to multiple chemotherapeutic agents due to its lower IC50 values. In conclusion, this study presents the first signature for predicting the prognosis and immunological status of CRC patients based on HSF family genes. Our findings suggest that HSF4 may serve as a potential therapeutic target in CRC.

cancer biology↗

bioRxiv2025

GABA-independent activation of GABAB receptor by mechanical forces

The heterodimeric GABAB receptor, composed of GB1 and GB2 subunits, is a metabotropic G protein-coupled receptor (GPCR) activated by the neurotransmitter GABA. GABA binds to the extracellular domain of GB1 to activate G proteins through GB2. Here we show that GABAB receptors can be activated by mechanical forces, such as traction force and shear stress, in a GABA-independent manner. This GABA-independent mechano-activation of GABAB receptor is mediated by a direct interaction between integrins and the extracellular domain of GB1, indicating that GABAB receptor and integrin form a novel type of mechano-transduction complex. Mechanistically, shear stress promotes the binding of integrin to GB1 and induces an allosteric re-arrangement of GABAB receptor transmembrane domains towards an active conformation, culminating in receptor activation. Furthermore, we demonstrate that shear stress-induced GABAB receptor activation plays a crucial role in astrocyte remodeling. These findings reveal a previously unrecognized function of GABAB receptor in mechano-transduction, uncovering a novel ligand-independent activation mechanism for GPCRs.

neuroscience↗

bioRxiv2025

Mechanical force-mediated cellular crosstalk maintains the integrity of the lung gas exchange niche

Respiratory motion imposes a constant mechanical strain that has important but poorly defined impact on tissue niches in the lung. We developed a reversible bronchial ligation model to induce and reverse unilateral blockade of lung mechanical motion in vivo and show that this leads to transcriptomic changes in multiple cell lineages that are not normalized upon reinitiation of respiratory motion. Perturbation of mechanosignaling specifically in alveolar epithelial type I (AT1) cells alters the transcriptomic state and fate of their niche neighbors, demonstrating that AT1 cells act as a node that propagates a mechanical cascade throughout the lung alveolus. Mechanically perturbed AT1 cells induce a distinct capillary endothelial cell state that persists after reactivation of respiratory motion, which is mediated by an integrin/TGF-{beta} network within the alveolus that is vulnerable to pharmacological intervention. Importantly, AT1 mechanosignaling and intercellular communication are altered in chronic human lung diseases, highlighting the critical role of an AT1-driven mechanosensing network in lung disease biology. Thus, mechanosensing cells propagate biophysical signals that regulate tissue function and program tissue responses in disease.

cell biology↗

bioRxiv2025

Leveraging autophagy and pyrimidine metabolism to target pancreatic cancer

Autophagy inhibitors are promising compounds to treat pancreatic ductal adenocarcinoma (PDA) but their efficacy in patients is unclear, highlighting a need to understand mechanisms of resistance. We used a novel approach to uncover metabolic adaptations that bypass autophagy inhibition. Utilizing PDA cells with acquired resistance to different autophagy inhibitors, we found that severe autophagy depletion induces metabolic rewiring to sustain TCA intermediates and nucleotides for biosynthesis. Long-term autophagy inhibition results in altered pyruvate metabolism likely regulated by lower pyrimidine pools. Cells adapting to loss of autophagy preferentially salvage pyrimidines to replenish these pools instead of synthesizing them de novo. Exploiting this metabolic vulnerability, we found that acquired resistance to autophagy inhibition promotes increased salvage and therefore sensitivity to pyrimidine analogues, including gemcitabine and trifluridine/tipiracil leading to combinatory effects with autophagy inhibitors and pyrimidine analogs. These studies provide mechanistic insight defining how autophagy inhibition can be leveraged to treat pancreatic cancer.

cancer biology↗

bioRxiv2025

Design of combination therapeutics from protein response to drugs in ovarian cancer cells

High-grade serous ovarian cancer (HGSOC) remains the most lethal gynecologic malignancy, and novel treatment approaches are needed. Here, we used unbiased quantitative protein mass spectrometry to assess the cellular response profile to drug perturbations in ovarian cancer cells for the rational design of potential combination therapies. Analysis of the perturbation profiles revealed proteins responding across several drug perturbations (called frequently responsive below) as well as drug-specific protein responses. The frequently responsive proteins included proteins that reflected general drug resistance mechanisms, such as changes in drug efflux pumps. Network analysis of drug-specific protein responses revealed known and potential novel markers of resistance, which were used to rationalize the design of anti-resistance drug pairs. We experimentally tested the anti-proliferative effects of 12 of the proposed drug combinations in 6 HGSOC cell lines. While response typically varies across different cell lines, 10 of the 12 combinations tested have either an additive or synergistic CI index in at least one cell line and may therefore be plausible candidates for overcoming or preventing resistance to single agents. Serendipitously, we observed an unexpectedly strong 0.05-0.11 micromolar response to GPX4 inhibitors as single agents in the OVCAR-4 cell line. We propose several drug combinations as potential therapeutic candidates in ovarian cancer, as well as GPX4 inhibitors as single agents. HighlightsO_LI5000-protein response to 7 drugs in an ovarian cancer cell line profiled by protein mass spectrometry C_LIO_LINetwork analysis suggested potential pathways of drug resistance inferred from response profiles C_LIO_LIDemonstration of a general method for profiling adaptive response to therapeutic interventions with implications for the development of anti-resistance therapy C_LIO_LIPlausible anti-resistance drug combinations tested for antiproliferative effect in up to 6 ovarian cancer cell lines C_LIO_LIDrug combinations with additive or synergistic antiproliferative effects are plausible pre-clinical candidates for overcoming or preventing resistance to single agents C_LIO_LISeveral combinations were synergistic in some cell lines (with PARPi, MEKi, and SRCi) C_LIO_LIWe observed 0.05-0.11 micromolar response to GPX4 inhibitors as single agents in the OVCAR-4 cell line C_LI

cancer biology↗

bioRxiv2025

DNA2 and MSH2 activity collectively mediate chemically stabilized G4 for efficient telomere replication

G-quadruplexes (G4s) are widely existing stable DNA secondary structures in mammalian cells. A long-standing hypothesis is that timely resolution of G4s is needed for efficient and faithful DNA replication. In vitro, G4s may be unwound by helicases or alternatively resolved via DNA2 nuclease mediated G4 cleavage. However, little is known about the biological significance and regulatory mechanism of the DNA2-mediated G4 removal pathway. Here, we report that DNA2 deficiency or its chemical inhibition leads to a significant accumulation of G4s and stalled replication forks at telomeres, which is demonstrated by a high-resolution technology: Single molecular analysis of replicating DNA (SMARD). We further identify that the DNA repair complex MutS (MSH2-MSH6) binds G4s and stimulates G4 resolution via DNA2-mediated G4 excision. MSH2 deficiency, like DNA2 deficiency or inhibition, causes G4 accumulation and defective telomere replication. Meanwhile, G4-stabilizing environmental compounds block G4 unwinding by helicases but not G4 cleavage by DNA2. Consequently, G4 stabilizers impair telomere replication and cause telomere instabilities, especially in cells deficient in DNA2 or MSH2.

molecular biology↗

bioRxiv2025

Endoplasmic reticulum stress protein GRP78 for ketamine's antidepressant effects

Ketamine is a fast-acting, long-lasting novel antidepressant. However, underpinning intracellular mechanisms remain unclear. We conducted an unbiased screening for genes that were less expressed in the prefrontal cortex (PFC) of mice that did not display antidepression-like effects to ketamine. GO analysis implicated endoplasmic reticulum and protein folding; in particular, GRP78, a stress-induced chaperone protein critical for protein folding, was reduced. We showed that GRP78 deficiency in PFC neurons induced depressive-like behaviors, whereas its overexpression produced anti-depression-like effects, revealing a novel function of GRP78. Prefrontal GRP78 was necessary for ketamines antidepressant-like effects. GRP78 was also required for ketamine to increase calcium activity and glutamatergic transmission. Enhancing GRP78 by viral infection and azoramide enabled non-responsive mice to respond to ketamine. Together, our results demonstrate that GRP78 is critical for ketamine to execute antidepressant effects by potentiating glutamatergic transmission in the PFC. HighlightsO_LIGRP78 was identified in non-biased screens for proteins that were lower in the PFC of mice that failed to exhibit antidepression-like effects after ketamine. C_LIO_LIReducing GRP78 in the PFC induced depressive-like behaviors while increasing GRP78 had opposite effects in wildtype mice. C_LIO_LIGRP78 is required for ketamine to increase calcium activity in excitatory neurons and glutamatergic transmission. C_LIO_LIEnhancing GRP78 by viral infection and by azoramide enabled non-responsive mice to respond to ketamine. C_LI

neuroscience↗

bioRxiv2024

Beta-DIA: Integrating learning-based and function-based feature scores to optimize the proteome profiling of single-shot diaPASEF mass spectrometry data

We present a freely available diaPASEF data analysis software, Beta-DIA, that utilizes deep learning methods to score coelution consistency in retention time-ion mobility dimensions and spectrum similarity. Beta-DIA integrates these learning-based scores with traditional function-based scores, enhancing the qualitative analysis performance. In some low detection datasets, Beta-DIA identifies twice as many protein groups as DIA-NN. The success of Beta-DIA has paved another way for the application of deep learning in fundamental proteome profiling.

bioinformatics↗

bioRxiv2024

TIPP3 and TIPP3-fast: Improved Abundance Profiling in Metagenomics

We present TIPP3 and TIPP3-fast, new tools for abundance profiling in metagenomic datasets. Like its predecessor, TIPP2, the TIPP3 pipeline uses a maximum likelihood approach to place reads into labeled taxonomies using marker genes, but it achieves superior accuracy to TIPP2 by enabling the use of much larger taxonomies through improved algorithmic techniques. We show that TIPP3 outperforms leading methods for abundance profiling in two important contexts: when reads come from genomes not already in a public database (i.e., novel genomes) and when reads contain sequencing errors. We also show that TIPP3-fast has slightly lower accuracy than TIPP3, but is still more accurate than other leading methods and uses a small fraction of TIPP3s runtime. Additionally, we highlight the potential benefits of restricting abundance profiling methods to those reads that map to marker genes (i.e., using a filtered marker-gene based analysis), which we show typically improves accuracy. TIPP3 is freely available at https://github.com/c5shen/TIPP3. Author summaryTIPP3 is a new marker gene-based abundance profiling tool that builds on TIPP and TIPP2 with significant enhancements. TIPP3 supports larger reference packages ([~] 55,000 sequences per marker gene) and achieves higher accuracy in abundance profiling, especially with challenging input reads containing sequencing errors or novel genomes. TIPP3 outperforms TIPP2 and other leading methods in profiling accuracy, and its fast version TIPP3-fast is competitive in runtime with the competing methods while being more accurate under challenging conditions. TIPP3 is open-source and available at https://github.com/c5shen/TIPP3.

bioinformatics↗

bioRxiv2024

Dynamic epigenomic landscape of carbon-concentrating mechanisms in the model industrial oleaginous microalga Nannochloropsis oceanica

Despite their ecological and physiological significance, how carbon-concentrating mechanisms (CCM) are regulated in microalgae remains elusive. Here in the model industrial microalga Nannochloropsis oceanica, we uncovered an epigenetic regulatory mechanism for CCM via comprehensive, multi-dimensional epigenomic analyses. Our integrated study reveals the complex interplay among histone modifications, dynamic nucleosome positioning, and 3D chromatin structure in regulating gene expression during low CO2 adaptation, despite minimal DNA methylation. Histone modifications, including lysine acetylation (H3K9ac and H3K27ac), crotonylation (Kcr), and methylation (H3K4me2), were associated with active chromatin states. Significantly altered ChIP-Seq peaks were linked to 43.1% of the differentially expressed genes (DEGs). Notably, H3K4me2 exhibited a distinct dual-peak profile around the transcription start site (TSS), which is unique among microalgae and plants. Chromatin compartment dynamics were correlated with gene expression and histone modifications, particularly H3K4me2, while differentially positioned nucleosomes were associated with key CCM-related genes and transcription factors. To further elucidate the role of H3K4me2, we knocked out its methyltransferase, resulting in genome-wide H3K4me2 peak shifts, slower growth, and reduced photosynthesis. These changes were accompanied by differential expression of key genes of NoHINT and NoPMA2, whose subsequent deletion and overexpression revealed their subtle yet significant impacts on growth and photosynthetic efficiency under low CO2 conditions, with NoHINT regulating growth and NoPMA2 influencing photosynthesis. Finally, we proposed a comprehensive model for epigenetic regulation of CCM in N. oceanica, which established a foundation for enhancing microalgal productivity through targeted epigenetic modifications. HighlightsO_LIMulti-layered epigenetic modifications contribute to the regulation of CCM and its adaptation to low CO2 in N. oceanica. C_LIO_LIThe histone modification H3K4me2 regulates the growth and photosynthesis of N. oceanica under low CO2 conditions. C_LIO_LIH3K4me2 targets NoHINT and NoPMA2 in N. oceanica, with NoHINT influencing growth dynamics and NoPMA2 modulating photosynthetic efficiency under low CO2 conditions. C_LI

genomics↗

bioRxiv2024

DOCK8 regulates a mechanosensitive actin redistribution that maintains immune cell cohesion and protects the nucleus during migration

Immune cells navigate through complex 3-dimensional tissue architectures, utilizing an amoeboid mode of migration, characterized by extensive cellular deformation, low adhesion, and high cell velocities. In the absence of expression of Dedicator of Cytokinesis 8 (Dock8), a gene identified with loss-of-function mutations in immunodeficiency, cells become entangled during migration through dense, confined environments and consequently undergo catastrophic cell rupturing, while migration on 2D surfaces remains entirely intact. Here we investigated the specific cytoskeletal defect of Dock8-deficient activated T cells, showing that even prior to entanglement they display a striking difference in F-actin distribution compared to wild type (WT) cells. We describe a central pool of F-actin in WT murine and human T cells which is absent in Dock8 KO T cells, and determine that the relocalization of F-actin is a mechanoresponsive circuit, emerging only when cells are very confined. Our works shows that the central actin pool is nucleo-protective, reducing nuclear deformation and DNA damage during confined migration. We identify the Hippo-pathway kinase Mst1 as a co-mediator of this mechanosensitive pathway in conjunction with Dock8, allowing for cell cohesion and survival during migration through complex environments.

immunology↗

bioRxiv2024

A unique mechanism of snRNP core assembly

The assembly of spliceosomal snRNP cores involves seven Sm proteins (D1/D2/F/E/G/D3/B) forming a ring around each snRNA and typically requires several essential assembly chaperones, particularly the SMN-Gemins complex implicated in spinal muscular atrophy (SMA). Strikingly, in budding yeast, snRNP core assembly only involves Brr1, a nonessential homolog of Gemin2. To unravel this enigma, we systematically investigated snRNP core assembly in budding yeast using biochemical and genetic approaches. We discovered two distinct pathways in budding yeast: chaperone-mediated and direct. The chaperone-mediated pathway involves two proteins, Brr1 and a novel protein, Lot5, but is inefficient. Lot5 binds D1/D2/F/E/G to form a heterohexameric ring (6S). Brr1 binds D1/D2/F/E/G and 6S but cannot displace Lot5 to facilitate assembly. Disruption of both BRR1 and LOT5 genes caused mild growth retardation, but LOT5 overexpression substantially impeded growth. The direct pathway uniquely involves F/E/G as a trimer and a stable D1/D2/F/E/G intermediate complex, explaining the non-essentiality of assembly chaperones. These findings unveil a unique assembly mechanism of snRNP cores, illuminate the evolution of assembly chaperones, and suggest avenues for studying SMA pathophysiology.

molecular biology↗

bioRxiv2024

Stearoyl coenzyme A desaturase 1 (SCD1) regulates foot-and-mouth disease virus replication by modulating host cell lipid metabolism and 2C-mediated replication complex formation

The life cycle of foot-and-mouth disease virus (FMDV) is tightly regulated by host cell lipid metabolism. In a previous study, we successfully established a BHK-21 cell model (BHK-Op) for persistent FMDV infection by single-cell clone selection and isolated a virus-negative cell line (BHK-VEC cells) from high-passage BHK-Op cells. BHK-VEC cells could be not infected with FMDV. By conforming the transcriptome data of BHK-VEC cells and BHK-21 cells, we identified that the stearoyl coenzyme A desaturase 1 (SCD1), a key enzyme for the fatty acid metabolism, regulates FMDV replication. SCD1 overexpression or exogenous addition of oleic acid (OA), a product of SCD1 enzyme activity, promoted or upregulated FMDV replication in BHK-21 cells or SCD1 knockdown cells, respectively. Interestingly, overexpression of SCD1 or exogenous addition of OA restored the FMDV infection and replication in BHK-VEC cells. Exogenous addition of OA also promoted FMDV replication in BHK-Op. SCD1 recruited the nonstructural FMDV protein 2C to the detergent-resistant membrane located in the perinuclear nucleus to form replication complex. Inhibition of SCD1 enzyme activity resulted in significantly decreased number of FMDV replication complexes with also abnormal morphology. Importantly, inhibition of SCD1 enzyme activity effectively suppressed replication of other positive-sense RNA viruses, such as REO176, PV1 and EV71. Our results demonstrated that, as a key host regulator of RNA virus replication, SCD1 is a potential target for developing novel drugs against positive-sense RNA virus infection.

microbiology↗

bioRxiv2024

Investigation of the mechanism of accelerated biodegradation of Paracoccus-KDSPL-02

Paracoccus-KDSPL-02 can accelerate to degrade penicillin G under light remain poorly understood, largely due to the lack of high-throughput genome engineering tools. Firstly, this study sequenced the genome of Paracoccus-KDSPL-02 and mined the genes that might be involved, and in order to understand in detail whether the expression of the mined genes changed during light. Further, for genes with altering transcriptional levels under light, this study obtained PROKKA_01468 which a photoreceptor protein in Paracoccus-KDSPL-02. In the end, for validating the function of PROKKA_01468, this study knocked down the sequence of the PROKKA_01468 by applying gene editing system, and the knockdown strain showed significant change in the rate of degradation of phenylacetic acid, which is the intermediate product of penicillin G degradation, by light compared with darkness, so that the PROKKA_01468 is the most effective photoreceptor protein in Paracoccus-KDSPL-02. SynopsisThis research elucidates a molecular mechanism capable of accelerating penicillin G degradation in wastewater, with significant implications for environmental science.

bioengineering↗