Biology subjects

Inoue, M.

Publications and source records attributed to Inoue, M..

At least 19 recordsLinked to original sources

bioRxiv2026

Sex Differences in Physiological Hair Cycling and Adhesive Material-Induced Hair Regeneration in Mice

Sex differences in hair growth are clinically evident, but sex-dependent regulation of physiological hair cycling and injury-induced hair regeneration remains incompletely understood. We compared physiological dorsal hair-cycle progression and adhesive material-induced localized hair regeneration in male and female C3H/He mice. Males entered the second and third anagen phases earlier than females, indicating longer telogen phases in females. In contrast, localized hair regrowth after application and removal of a cyanoacrylate adhesive material appeared earlier in females. Ovariectomy induced widespread telogen-to-anagen transition and therefore did not permit isolation of ovarian-hormone effects on the localized response. RNA sequencing of intact dorsal skin identified sex-dependent baseline expression profiles involving inflammation, wound response, and tissue repair. Independent time-course quantitative PCR further demonstrated sex-dependent expression of inflammatory and reparative genes after adhesive material application. Local clodronate liposome administration alone induced delayed perifocal hair growth. When combined with adhesive material application, clodronate treatment markedly delayed wound healing and localized hair regrowth in males, whereas these responses were comparatively preserved in females. These findings show that physiological hair cycling and adhesive material-induced hair regeneration exhibit distinct sex differences and suggest that the localized regenerative response is more macrophage-dependent in males than in females.

developmental biology↗

bioRxiv2026

Regional Differences in Dorsal Skin Determine the Rate of Adhesive Material-Induced Hair Regeneration

Dorsal skin is widely used in mouse wound-healing, dermatitis, and hair-cycle models, but is often treated as a uniform site. We investigated whether adhesive material (cyanoacrylate)-induced hair regeneration, a model we previously reported, differs by position within the dorsal skin. Adhesive material was applied to four regions along the cranial-to-caudal axis of the mouse dorsal skin. Hair regrowth appeared earlier at the cranial sites than at the caudal sites, and this difference persisted through late anagen and the anagen-to-catagen transition. In contrast, hair regrowth after full-thickness skin excision was slower, smaller in area, and less reproducible than that after adhesive material application. Expression of Hox genes, including Hoxa9, Hoxb9, Hoxc9, Hoxa10, and Hoxc10, was higher at the caudal sites than at the cranial sites but did not correlate with the timing of hair regrowth. RNA sequencing of intact skin from the cranial and caudal sites revealed distinct baseline profiles, including differences in the Wnt inhibitor Sfrp4 and the adipogenic genes Ppar{gamma} and Fabp4. Early after adhesive material application, histological changes and the expression of inflammation- and tissue-repair-related genes also differed between the cranial and caudal skin. These findings indicate that mouse dorsal skin is not a uniform experimental field and that cranial-to-caudal position should be considered when designing and interpreting hair-regeneration and wound-healing experiments in mice.

developmental biology↗

bioRxiv2026

BMP-3b suppresses proliferation, migration, invasion, and TGF-β 1/Smad3 signaling in breast cancer cells

ObjectiveBone morphogenetic protein-3b (BMP-3b), also known as growth differentiation factor 10, has been implicated in tumor suppression; however, its role in breast cancer and its interaction with transforming growth factor-{beta}1 (TGF-{beta}1) signaling remain incompletely understood. MethodsPublicly available datasets were used to examine BMP-3b expression in breast lesions and its association with overall survival in patients with stage III or IV breast cancer. Human MCF-7 and murine 4T1 breast cancer cells were treated with recombinant BMP-3b. Cell proliferation, migration, invasion, epithelial-mesenchymal transition-related proteins, and TGF-{beta}1-induced Smad3 phosphorylation were assessed using Cell Counting Kit-8, scratch wound-healing, Transwell invasion, and Western blot assays. ResultsBMP-3b expression was lower in ductal carcinoma in situ than in normal mammary tissue. Low BMP-3b expression was associated with poorer overall survival in patients with stage III or IV breast cancer. BMP-3b reduced proliferation of MCF-7 and 4T1 cells and inhibited migration and invasion of 4T1 cells. BMP-3b increased E-cadherin and decreased vimentin expression in both cell lines. It also attenuated TGF-{beta}1-induced migration, invasion, and Smad3 phosphorylation in 4T1 cells. ConclusionsBMP-3b suppresses malignant phenotypes of breast cancer cells and modulates TGF- {beta}1/Smad3 signaling. These findings identify BMP-3b as a potential endogenous regulator of breast cancer progression.

cell biology↗

bioRxiv2026

Co-folding of Membrane Proteins and Lipid Molecules Improves Membrane-Protein Structure Prediction Accuracy

Recent advances in deep-learning-based structure prediction have greatly improved the accuracy of protein structure modeling and enabled prediction of biomolecular complexes. However, the surrounding molecular environments are typically not represented explicitly, and their effects are therefore captured only implicitly. This limitation is particularly relevant for membrane proteins, whose structures and interactions are strongly influenced by the membrane environment. Here we introduce co-folding of membrane proteins and lipid molecules (CoMPLip), a method that imposes an explicit membrane context by co-folding proteins with lipid molecules during AlphaFold 3 (AF3) predictions. In CoMPLip, lipid molecules arrange into bilayer-like configurations around transmembrane regions, providing a membrane-like environment during structure prediction. Across benchmark datasets of ligand-bound membrane proteins, full-length single-pass membrane proteins, and dynamic transporters, CoMPLip improves ligand-pose prediction, promotes correct extracellular-intracellular domain separation, and enables sampling of multiple conformational states. CoMPLip is training-free and is compatible with the existing AF3 workflows.

bioinformatics↗

bioRxiv2026

The Nkx2.3-Nr5a1 gene cascade plays a crucial role in spleen-specific vascular architecture and marginal zone formation

NR5A1 is a nuclear receptor and master regulator of steroidogenic tissue development and steroid hormone biosynthesis in the adrenal glands and gonads. Although NR5A1 is expressed in splenic vascular endothelial cells, its function in the adult spleen remains unclear. Using single-cell transcriptomics in mice, we show that NR5A1-positive endothelial cells are heterogeneous and exhibit distinct phenotypes according to their localization in the splenic sinus or marginal sinus. To assess NR5A1 function, we generated a spleen-specific Nr5a1 enhancer deletion model. Enhancer loss resulted in reduced spleen size and ablation of the marginal zone and marginal sinus. In addition, 21-hydroxylase activity in splenic sinusoidal endothelial cells was reduced, particularly in females, leading to decreased levels of adrenocortical steroids in the spleen. Enhancer deletion also induced ectopic lymphatic-like and high endothelial venule-like vasculature similar to those observed in Nkx2.3-deficient mice. Consistently, mutation of the NKX2.3-binding motif within the enhancer abolished NR5A1 expression. Together, these findings identify an Nkx2.3[->]Nr5a1 regulatory axis essential for spleen-specific endothelial cell differentiation and splenic architecture required for blood filtration and marginal zone formation.

developmental biology↗

bioRxiv2026

Modeling Time to Visual Insight in Mooney Image Recognition with a Chaotic Recurrent Neural Network

Insight is often described as a sudden shift in or formation of a conceptual representation, enabling humans to restructure existing knowledge and solve problems beyond conventional analytical approaches. Although prior computational studies have modeled aspects of insight using deep neural networks (DNNs) or reinforcement learning, few have captured the dynamic emergence of insight through autonomous neural computation. Here, we present a neural network model that simulates the time required to reach visual insight in the Mooney image recognition task, a widely used paradigm for studying visual insight and perceptual reorganization. The model couples a DNN module for perceptual feature extraction with a recurrent neural network (RNN) that implements a chaotic search process for recognition. The RNN is formulated as a continuous-time dynamical system, autonomously explores internal states, and stabilizes when the missing visual features required for recognition are internally reconstructed. Using the same image set as in human psychophysical experiments, the model reproduces key statistical properties of human search times (STs), including (i) lognormal-like ST distributions across participants for each image, (ii) a proportional relationship between the log-scale mean and standard deviation estimated from lognormal fits across images, and (iii) discrete levels of the fitted log-scale mean across images (a proxy for image difficulty). Importantly, these properties emerge without assuming any lognormal distribution for participant-to-participant variability, whereas previous models reproduced similar signatures by positing lognormal-distributed individual differences. We further show that lognormal-like signatures can arise from exponential search dynamics when combined with both standard experimental preprocessing and finite observation windows, highlighting the need to distinguish generative mechanisms from measurement and analysis effects. Together, these results motivate a mechanistic link between chaotic neural dynamics and insight-related search and provide a computational framework for implementing insight in artificial systems.

neuroscience↗

bioRxiv2025

Ataxia-Telangiectasia Mutated Inhibition Enhances Adeno-Associated Virus-Mediated Knock-in Efficiency in Pig Zygotes

A persistent global shortage of transplantable organs has renewed interest in pigs as donors for xenotransplantation and hosts for interspecies organogenesis considering their physiology closely resembles that of humans. Such applications require pigs harboring genetic modifications, including knockouts, human transgenes, and conditional alleles. Although such complex allele combinations can be assembled by sequential editing of fetal fibroblasts, followed by somatic cell nuclear transfer (SCNT), SCNT is often associated with developmental abnormalities. Direct genome editing of pig zygotes offers an alternative route; however, achieving long-fragment knock-in, particularly at multiple loci, remains challenging. Here, adeno-associated virus (AAV) donor vectors for long-fragment knock-in in pig zygotes were evaluated, and tested whether transient inhibition of ataxia-telangiectasia mutated (ATM), which becomes overactivated during AAV transduction, could enhance knock-in efficiency. AAV6 donors supported efficient ACTB-mEGFP knock-in (33%), whereas short-term treatment with the ATM inhibitor AZ32 increased the efficiency to 66%. In addition, AZ32 enhanced simultaneous double knock-in at ACTB and UBB, generating a higher proportion of double-positive blastocysts (52% vs. 19% in controls), without affecting blastocyst formation rates or total cell numbers. Embryo transfer yielded ACTB-mEGFP and UBB-mScarlet-I3 double knock-in fetuses (33%), including an F0 fetus composed almost entirely of double knock-in cells. These results demonstrate that combining AAV donors with transient ATM inhibition is an efficient strategy for long-fragment knock-in at multiple loci in pigs.

bioengineering↗

bioRxiv2025

Seeing from the inside out: Intrinsic neural dynamics explain individual differences in movie watching

When viewing the same movie, individuals attend to different visual elements and construct distinct narratives. We hypothesized that these differences arise partly from intrinsic neural dynamics that specify upcoming visual content before eye movements occur, particularly when external visual saliency is low. Using fMRI and eye-tracking during a two-hour movie (n=12), we examined spontaneous gaze shifts during low versus high visual saliency periods. During low-saliency periods, when inter-individual variability was greatest, we found that visual features of upcoming gaze targets 2 seconds before eye movements could be predicted by right temporo-parieto-occipital junction (R-TPOJ) activity. Critically, the strength of connectivity between R-TPOJ and the right superior parietal lobule, which predicts gaze position, correlated with gaze-shift frequency during low-saliency periods. These findings suggest that R-TPOJ specifies the next scene content prior to foveation, and that eye movements serve to align this internally specified content with external stimuli, thereby shaping individual differences during movie-watching.

animal behavior and cognition↗

bioRxiv2025

Multiheme selenoenzyme essential for elemental sulfur respiration

Microbial reduction of elemental sulfur is a pivotal process in the global sulfur cycle1. Insoluble elemental sulfur can serve as a terminal electron acceptor during anaerobic respiration, producing sulfide2,3. However, the molecular mechanisms underlying sulfur reduction remain poorly understood. Here we show that an evolutionarily conserved multiheme cytochrome c selenoprotein (MccSep) is essential for elemental sulfur reduction in a sulfur-respiring bacterium. Our biochemical and structural analyses revealed that MccSep comprises four identical subunits, each containing five c-type hemes and one selenocysteine residue (U325). The enzyme catalyzes polysulfide reduction at a unique active site, where C239 coordinates with the heme iron center, while U325 plays a crucial role in the catalytic process. Genetic analysis further revealed the critical roles of U325 and C239 in driving in vivo elemental sulfur respiration. These findings unveiled a selenium-sulfur-dependent catalytic chemistry on a heme center during polysulfide reduction, expanding the scope of biological catalysis and deepening our molecular understanding of bacterial sulfur respiration.

microbiology↗

bioRxiv2025

Structural basis of lipid-mediated gating in a two-pore domain potassium channel

TOK1 is the first identified member of the K2P channel family and contains additional N- and C-terminal domains, displaying a configuration distinct from that of canonical K2P channels. Although recent advances in structural studies of K2P channels have elucidated their architectures, the structural basis of TOK1 has remained unknown, limiting our understanding of its unique configuration. Here, we present the cryo-electron microscopy (cryo-EM) structure of TOK1, unveiling its distinctive domain architecture. Furthermore, the structures of TOK1 in three distinct states provide mechanistic insights into its regulation through lipid binding and dissociation. Phosphorylation of TOK1 induces the formation of an additional lipid-binding site, leading to channel inactivation. Conversely, upon activation, the phospholipid dissociates, allowing ion permeation. Our comprehensive study, integrating cryo-EM structural analysis, molecular dynamics simulations, electrophysiological recordings, and mass spectrometry, elucidates the distinctive features of TOK1, an atypical K2P channel, and provides a framework for understanding lipid-mediated regulation within this family.

molecular biology↗

bioRxiv2025

Carbon monoxide-driven proton respiration enables facultative anaerobes to survive electron acceptor limitation

Diverse microorganisms couple the oxidation of carbon monoxide gas (CO) to the reduction of protons, producing hydrogen gas (H2). This energy-conserving process is mediated by the nickel-containing CO dehydrogenase/energy-converting hydrogenase (Ni-CODH/ECH). Yielding only a small supply of energy, the physiological role of this process at environmentally relevant CO levels remains unresolved. Here, we show that Ni-CODH/ECH enables metabolically flexible facultative anaerobes within the Anoxybacillaceae to survive electron acceptor limitation. Analysis of 387 Anoxybacillaceae genomes revealed that Ni-CODH/ECH had a patchy distribution and, with one exception, was mutually exclusive with the aerobic molybdenum-containing CODH. Culture experiments using the three isolates (Parageobacillus sp. G301, P. thermoglucosidasius NBRC 107763, and Thermolongibacillus altinsuensis B1-1) demonstrated that CO-dependent proton respiration is activated during stationary phase when exogenous electron acceptors are limiting, enhancing cell density 1.2-to 1.5-fold under 25% CO, whereas no effect was observed in a Ni-CODH knockout ({Delta}cooCSF) strain. RNA-seq analysis of strain G301 under twelve conditions revealed that Ni-CODH genes reached 2,000-12,500 TPM (top 0.2-1.9% of all genes) during stationary phase, independent of CO presence, under the predicted control of the redox-dependent transcriptional repressor Rex. {Delta}cooCSF cultures accumulated more trace CO than the wild-type, suggesting trace CO uptake by the wild-type. Thus, Ni-CODH/ECH is a redox-regulated auxiliary energy-conservation system that supports adaptation to electron acceptor limitation. Given the continual environmental supply of the two substrates for this enzyme, we propose CO-dependent proton respiration is a dependable way for metabolically flexible microorganisms to stay energized in spatiotemporally variable environments. Significance statementMicroorganisms are frequently challenged to survive in environments where both energy sources and electron acceptors are limited. We reveal that facultative anaerobes activate a respiratory process that utilizes carbon monoxide (CO) and protons to survive under electron acceptor limitation. This hydrogenogenic CO-oxidizing reaction, termed CO-dependent proton respiration, is catalyzed by an ancient and minimal complex, the nickel-containing CO dehydrogenase/energy-converting hydrogenase. Although the reaction yields barely enough energy to translocate protons, this complex provides a reliable lifeline by extracting energy from trace CO and protons that are ubiquitous in nature, even when other electron acceptors are depleted. The widespread distribution of this complex across bacteria and archaea suggests that it provides a universal adaptive advantage for life under energy-limited conditions.

microbiology↗

bioRxiv2025

IGF2BP3 is essential for the growth heterogeneity of colorectal adenoma cells by regulating MYC

Adenoma is a major precancerous lesion in colorectal cancer (CRC), and the adenoma-carcinoma sequence is a well-known multistep progression to CRC caused by the accumulation of genetic mutations. On the other hand, the non-genetic mechanisms in the adenoma-carcinoma sequence remain largely unknown. In this study, organoids were established from 31 colorectal adenomas from 19 patients. Some adenomas showed heterogeneity in the proliferative potential of single cells, and this heterogeneity was regulated by non-genetic mechanisms. IGF2BP3 was identified as a differentially expressed gene between organoids with different growth patterns. IGF2BP3 positively regulated MYC expression at the transcriptional level and negatively regulated it at the translational level. This promoted high proliferative potential with high levels of oxidative phosphorylation, while allowing cells to avoid MYC-induced cell death. IGF2BP3 affected the tumorigenicity of mouse adenomas in vivo. Intra-tumor heterogeneity in growth potential is acquired at the precancerous stage in the adenoma-carcinoma sequence of colorectal carcinogenesis, and IGF2BP3 plays an important role in regulating MYC levels. These findings provide new insights into the non-genetic regulation of adenomas during CRC development.

cancer biology↗

bioRxiv2025

The sympathoadrenal contribution to inferior vena cava formation

Vascular development is fundamental during embryogenesis. Although the molecular and cellular mechanisms of vascular formation have been extensively studied, the developmental basis common to anatomical variations in major veins remains poorly understood1-4. In particular, the renal segment of the inferior vena cava (IVC) exhibits marked anatomical variability, and these structural differences often affect the safety of retroperitoneal surgeries5,6. Here we show that the renal segment of the IVC in mouse embryos does not arise from the subcardinal vein (SubCV), as classically proposed7, but instead forms from a vascular plexus in the para-aortic ridge (PAR) closely associated with developing sympathetic and adrenal tissues. Three-dimensional imaging with molecular markers revealed the vascular plexus in PAR arises independently of the SubCV and develops in Zuckerkandl organ and adrenal gland primordia. Moreover, genetic models demonstrated that the development of the sympathetic and adrenal tissues contributes to the organization and remodeling of this vascular network. This sympathoadrenal contribution contrasts with the classical mesonephros-centric model and explains the consistent IVC structures observed even in the absence of renal development. Our findings suggest a mammal-specific mode of IVC formation driven by the emergence of dominant sympathetic paraganglia and reduced reliance on mesonephric filtration. This revised developmental framework provides insight into the evolutionary divergence of venous anatomy and may help interpret clinically significant vascular variations during abdominal surgery.

developmental biology↗

bioRxiv2025

The circulating cell-free DNA landscape in sepsis is dominated by impaired liver clearance

Circulating cell-free DNA (cfDNA) is a promising molecular biomarker. However, its utility in severe infection remains poorly understood. Here, we isolated cfDNA from sepsis patients and controls, demonstrating a 41-fold increase in the amount of cfDNA in circulation during disease. We used sequencing to reconstruct cfDNA methylomes, fragmentation profiles, and nucleosome footprints across 56 samples. We observed no difference in cfDNA composition between patients and controls, challenging the idea that cfDNA increases due to higher immune cell death during sepsis. Instead, we suggest that liver dysfunction prevents efficient clearance of cfDNA during disease. This was supported by fragmentation and end-motif patterns, both of which showed evidence of cfDNA being exposed to circulating nucleases for a prolonged period, proportionally to the extent of liver dysfunction. Variation in cfDNA of megakaryocyte-erythroid progenitor origin was also a significant contributor in sepsis, increasing over time. Moreover, we showed that cfDNA retains nucleosome footprints with cell type-specific gene activity information. We developed a novel approach to study nucleosome phasing that successfully recovers tissue-specific signatures. By combining this with single-cell data, we demonstrated that sepsis patients with liver dysfunction have higher amounts of cfDNA derived from Kupffer cells and the liver parenchyma. In conclusion, we present the first high-throughput multi-modal study of cfDNA during sepsis, which will serve as a reference point for future studies on the role of this biomarker in critical illness.

genomics↗

bioRxiv2025

PU.1 and TGF-β signaling transactivate CD103 expression in mast cells and dendritic cells: Opposite roles of GATA2 in the expression of mucosal mast cell-specific genes

Mucosal mast cells (MMCs) are distinguished from connective tissue MCs by the specific expression of integrin CD103 (E/{beta}7) and MC proteases Mcpt1 and Mcpt2. Although the expression of the Mcpt1 and Mcpt2 genes is cooperatively regulated by the transcription factor GATA2 and TGF-{beta} signaling in MMCs, the transcriptional mechanism of CD103 expression remains unknown. Here, we found that surface CD103 and Itgae mRNA levels were significantly increased by the knockdown (KD) of Gata2 in bone marrow-derived MCs (BMMCs), which was accelerated by a TGF-{beta} stimulation. Since the mRNA levels of Spi1 (encoding PU.1) were increased in Gata2 KD BMMCs, we examined the effects of PU.1 on CD103 expression. As expected, CD103 levels on BMMCs were significantly decreased by Spi1 KD and increased by Spi1 overexpression. Spi1 KD suppressed Itgae expression even in the presence of TGF-{beta} in BMMCs and peritoneal MCs, whereas Gata2 KD amplified the TGF-{beta}-induced increase in Itgae expression. The amount of PU.1 binding to the cis-element in the Itgae gene was significantly and moderately increased by Gata2 KD and the TGF-{beta} stimulation, respectively. Since PU.1 is an essential transcription factor for dendritic cells (DCs), we examined the role of PU.1 in CD103 expression on DCs. The KD experiment using BMDCs showed a significant decrease in CD103 levels in Spi1 siRNA-transfected BMDCs. We concluded that PU.1 affected CD103 expression on MMCs and DCs by transactivating the Itgae gene, and also that GATA2, which positively regulated the MMC-specific expression of Mcpt1 and 2, inhibited CD103 expression by repressing PU.1.

molecular biology↗

bioRxiv2025

Star-Shaped Glatiramer Acetate Mitigates Pulmonary Dysfunction and Brain Neurodegeneration in a Murine Model of Cryptococcus-Associated IRIS

Cryptococcal-associated immune reconstitution inflammatory syndrome (C-IRIS) is a clinical worsening or new presentation of cryptococcal disease following the initiation of antiretroviral therapy. C-IRIS is primarily driven by an influx of pathological CD4+ T cells, which triggers a hyperinflammatory response. The murine model of C-IRIS is a way to study the disease in mice and understand how the immune system triggers life-threatening outcomes in patients. We previously developed a murine C-IRIS model and demonstrated that C-IRIS is triggered by pathological CD4+ T cells, particularly Th1 cells, in the brain, which triggers neurodegeneration and pulmonary dysfunction. Using this unique mouse model, we tested the therapeutic effect of a star-shaped glatiramer acetate (sGA), which is a more effective isomeric form than linear GA. Here, we observed that sGA suppresses Th1 differentiation in the lung tissues, reducing CD4+ T cell and Th1 cell count. It also reduced microglia populations in the brain. Together, these changes improved respiratory dysfunction caused by C-IRIS, lowered mortality rate, and reduced brain neurodegeneration. These findings suggest that sGA could be an effective therapeutic strategy for managing C-IRIS.

immunology↗

bioRxiv2024

Implication of S-1 biomarkers on aging and prognosis in elderly patients with lung cancer treated by adjuvant S-1 chemotherapy: Accompanying results of the Setouchi Lung Cancer Group Study 1201

BACKGROUNDSThe management of elderly patients presents several challenges due to age-related declines; however recent recommendations advocate for age not being the sole determinant for adjuvant treatment decisions in patients with non-small cell lung cancer (NSCLC). Aging may alter expression levels of 5-fluorouracil (5-FU) biomarkers. METHODSExpression changes with aging were explored using The Cancer Genome Atlas (TCGA) database. 5-FU-related biomarker expressions, including thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyltransferase, epidermal growth factor receptor (EGFR), and excision repair cross-complementation group-1 (ERCC1), were assessed by the quantitative reverse-transcription PCR assays in 89 NSCLCs elderly patients ([≥] 75 years old) receiving adjuvant S-1, an oral fluoropyrimidine agent, therapy in a SLCG1201 trial. RESULTS: TCGA database analysis (n=955) indicated decreased TS expression with aging, particularly in those 75 or older. In the SCLG1201 trial, univariate analysis revealed that high EGFR and low TS expressions correlated with favorable recurrence-free survival (RFS)(p=0.0264) and overall survival (OS)(p=0.0365), respectively. Multivariable analysis confirmed pathological stage as an independent prognostic factor for both RFS and OS (p=0.0052 and 0.0352, respectively). EGFR mutant tumors (n=27) showed significantly higher DPD (p=0.0066) and EGFR (p<0.0001) expressions, and lower TS(p=0.0125) and ERCC1(p=0.0015) expressions. CONCLUSIONDespite pathological stage being an independent prognostic factor, high EGFR and low TS expressions may predict better clinical outcomes in elderly NSCLC patients using adjuvant S-1. The age-related decrease in TS expression supports the potential benefit of 5-FU-based therapy in them compared to younger patients. Further research is warranted to validate these clinical implications.

pharmacology and toxicology↗

bioRxiv2024

Barley is a potential trap crop for root parasitic weeds broomrapes

Root parasitic weeds broomrapes (Phelipanche and Orobanche spp.) cause devastating damages to agricultural production all over the world. The seeds of broomrapes germinate when they are exposed to germination stimulants, mainly strigolactones (SLs), released from roots of any plant species, while broomrapes parasitize only dicot plants. Therefore, monocots can be trap crops for broomrapes, as they induce seed germination but are not parasitized. In this study, we examined two European and one Japanese cultivars of barley for their potentials as trap crops for broomrapes and found that the European cultivars, Sebastian and Golden promise, are good potential trap crops as they produce more SLs and exhibit higher mycorrhizal colonization rates as compared to the Japanese cultivar Shunrai.

plant biology↗