Biology subjects

Shrestha, A.

Publications and source records attributed to Shrestha, A..

At least 19 recordsLinked to original sources

bioRxiv2026

Propidium monoazide (PMA) with quantitative PCR to detect and quantify viable Paenibacillus larvae and Melissococcus plutonius in honeybee hive samples

Paenibacillus larvae and Melissococcus plutonius are the bacterial agents responsible for American and European foulbrood diseases, respectively, and pose significant economic threats to apiculture worldwide. Early detection of these pathogens is critical for effective disease prevention and management in honeybee colonies. P. larvae forms highly persistent spores that can remain infectious on hive equipment for decades, whereas the non-spore-forming M. plutonius can survive for over a year in contaminated materials. Although various decontamination and treatment strategies are available or under development, reliable methods for quantifying these pathogens are essential for accurately assessing their effectiveness. Culture-based techniques and quantitative PCR (qPCR) are commonly used to detect and quantify foulbrood pathogens in hive-associated samples; however, culturing is labor-intensive and sometimes inconsistent, while qPCR does not distinguish between viable and dead cells. Propidium monoazide (PMA) selectively binds DNA from dead cells and prevents its amplification during qPCR, enabling viable-cell quantification. Despite this advantage, the performance of PMA-qPCR for detecting P. larvae and M. plutonius in hive samples has not previously been assessed. In this study, we evaluated PMA-qPCR using both pure cultures and environmentally relevant honeycomb samples before and after ozone treatment. PMA treatment greatly reduced the erroneous detection of dead cells by several orders of magnitude in both culture and hive samples, supporting its utility for AFB and EFB risk assessment and treatment evaluation. However, incomplete suppression of dead-cell DNA at high cell densities indicates that further optimization of PMA treatment conditions may be necessary.

microbiology↗

bioRxiv2026

Eukaryotic Initiation Factor 5B (eIF5B)-Driven Translational Control Impacts Oral Squamous Cell Carcinoma Pathophysiology

The non-canonical translation of specific mRNAs has been implicated in oncogenesis and cancer progression. We previously identified eukaryotic Initiation Factor 5B (eIF5B) as a key factor in Internal Ribosome Entry Site (IRES)-mediated translation of a subset of mRNAs encoding anti-apoptotic proteins. Here, we demonstrate that EIF5B is predominantly expressed in cancer cells compared to other cell types in the Oral Squamous Cell Carcinoma (OSCC) microenvironment. Higher EIF5B mRNA and protein expression are associated with poor patient outcomes. We show that eIF5B depletion in OSCC cells blunted pro-growth, pro-inflammatory, and pro-angiogenic signaling pathways and significantly increased TNF-related apoptosis-inducing ligand (TRAIL)-induced cell death. This is achieved through decreased translation of mRNAs encoding critical factors associated with OSCC pathophysiology. Importantly, the level of interaction of eIF5B with tRNAiMet was significantly higher in OSCC cells compared to non-cancerous fibroblasts. This suggests that OSCC cells (but not non-cancerous fibroblasts) rely heavily on eIF5B for translation initiation. In an in vivo flank xenograft model using nude mice, eIF5B knockdown in UMSCC-29 cells led to a significant reduction in tumor volume compared to control tumors. Also, the immunohistochemical analysis of the xenografted tumor sections demonstrated decreased staining intensity of critical factors associated with OSCC pathophysiology in eIF5B-depleted tumors relative to controls. Collectively, our data demonstrate that OSCC cells are uniquely dependent on eIF5B-tRNA interactions to sustain translation of pro-survival mRNAs. Targeting eIF5B disrupts these oncogenic programs, sensitizing OSCC cells to apoptosis and suppressing pro-angiogenic and pro-growth signaling.

cancer biology↗

bioRxiv2026

HvbZIP33 and HvbZIP76 have overlapping roles in foliar transpiration in drought-stressed barley

Basic leucine zippers (bZIP) constitute one of the biggest protein families and evolutionarily conserved transcription factors (TFs) in plants. We obtained mutant lines for two bZIP TFs, HvbZIP33 and HvbZIP76, in the genetic background of the barley cultivar Golden Promise (GP) via targeted gene-specific mutagenesis using an RNA-guided Cas9 endonuclease. A comprehensive morphological, physiological and transcriptomic analysis was performed in wild-type GP compared with hvbzip33 and hvbzip76 mutants under drought stress. The morphological and physiological changes were similar in both mutants and in the wild-type GP. Most strikingly, the mutants exhibited accelerated wilting and increased water loss. This effect was primarily caused by higher stomatal conductance (gs) and transpiration rate (E) in mutants compared to wild-type GP under both control and drought conditions, which in turn had a detrimental effect on the mutants intrinsic water use efficiency (iWUE). Likewise, the transcriptome profiles of hvbzip33 and hvbzip76 were more similar to each other than those of wild-type GP. We found that the number of differentially regulated genes under control versus drought-stress conditions was higher in the mutants than in wild-type GP, suggesting that the mutants try to compensate for accelerated foliar water loss. The study highlights the essential roles of HvbZIP33 and HvbZIP76 in balancing water loss in barley. These findings provide a foundation for engineering enhanced drought tolerance in barley through targeted manipulation of these genes to optimize transpiration rates.

genetics↗

bioRxiv2025

Hive-associated bacteria improve honeybee survival during Paenibacillus larvae infection

Honeybees (Apis mellifera L.) are the most common pollinators of crops. Honeybee larvae are susceptible to Paenibacillus larvae, a spore-forming Gram-positive bacterium that causes American Foulbrood (AFB), one of the most destructive brood diseases worldwide. Existing antibiotic treatments are undesirable due to increasing pathogen resistance and their residual accumulation in bee products. Consequently, there is increasing interest in biological agents and natural strategies for AFB control. However, most studies remain limited to in vitro or in vivo experiments and rarely evaluate impacts on adult bees. In this study, we systematically investigated hive-associated bacteria for their potential to enhance larval survival during P. larvae infection. Bacteria isolated from AFB-infected combs were sequenced and screened for antagonistic activity. Several Bacillus species--including B. zhangzhouensis, B. subtilis, B. amyloliquefaciens, B. licheniformis, and B. mojavensis--inhibited one or more P. larvae strains. Notably, the lysate of B. licheniformis suppressed all tested strains; Further characterization revealed that its main antibacterial component consists of heat-stable proteins between 30-50 kDa. Two Bacillus strains were selected for larval infection assays using laboratory-reared honeybee larvae: both significantly improved survival by 42% and 71%, respectively. To evaluate potential effects on adult bees, newly emerged workers were caged and fed B. licheniformis ASx lysate. Their survival differed from that of untreated controls but remained comparable to the Terra-Pro-fed bees, a Terramycin-based AFB treatment, and their gut microbiome remained similar to that of untreated controls. Overall, our findings suggest that hive-associated Bacillus species offer promising, low-impact candidates for AFB disease management.

microbiology↗

bioRxiv2025

Spatiotemporal remodeling of chromatin topology architecture and H3K27me3 redistribution underlies vascular pathology in Hutchinson-Gilford progeria syndrome

Hutchinson-Gilford progeria syndrome (HGPS) is a devastating premature aging disorder driven by the accumulation of the lamin A variant, progerin, leading to severe vascular pathology. While epigenetic alterations are implicated, the spatiotemporal reorganization of the higher-order chromatin and its functional impact on vascular smooth muscle cell (VSMC) transcription remain poorly defined. Through an integrated, longitudinal multi-omics approach combining in situ high-throughput chromosome conformation capture (Hi-C) and Cleavage Under Targets and Tagmentation (CUT&Tag) profiling of CTCF, SMC1A, H3K27me3, H3K27ac, and H3K36me3 with transcriptomic analyses from control and HGPS iPSC-derived VSMCs, we reveal that global topologically associating domain (TAD) architecture remains largely intact in HGPS. However, the internal chromatin states of TADs undergo dynamic, passage-specific remodeling, characterized by a progressive accumulation of broad H3K27me3-repressed domains. This is accompanied by a loss of A/B compartment segregation, as confirmed by DNA-FISH, and a pronounced depletion of interchromosomal intermingling, specifically surrounding downregulated genes, suggesting that these interchromosomal contacts are essential for maintaining transcriptional competence in normal VSMCs. Crucially, we uncover widespread rewiring of enhancer-promoter (E-P) loops, which is linked to the dysregulation of genes critical for vascular development, extracellular matrix organization, and atherosclerosis. Our study demonstrates that spatiotemporal redistribution of repressive histone marks and reorganization of E-P interactions within a structurally resilient TAD framework underpin widespread transcriptional dysregulation in HGPS vascular pathogenesis. This uncovers a critical dissociation between higher-order chromatin architecture and histone modification landscape, providing a mechanistic basis for the failure of vascular homeostasis in progeria.

genomics↗

bioRxiv2025

Bacteriophage density influences the rate of resistance evolution

The antagonistic relationship between bacteria and bacteriophages (phages) drives genetic changes that result in phage resistance. Phage resistance mutations arise in natural microbial communities and during the treatment of diseases with phages (phage therapy), making it important to understand the dynamics of resistance acquisition. It is well-established that when bacteria are challenged with phages in dense liquid cultures, bacterial populations quickly become dominated by phage-resistant variants. However, these conditions--well-mixed liquid cultures with high phage concentrations--are not necessarily common in microbial ecosystems. We developed a simplified mathematical model of phage resistance evolution to explore how phage and host concentration impact the dynamics of resistance evolution. The model was parameterized with microbial growth data from two pathogens and their phages: Pseudomonas aeruginosa and Paenibacillus larvae. Our analyses revealed two fundamental discoveries about resistance evolution. First, phage resistance evolution is predictably governed by a core set of parameters that exhibited high resolution across all bacterial strains: intrinsic growth rate of susceptible bacteria, resistance acquisition rate, fitness cost of resistance, and phage adsorption rate. Second, competitive interactions and fitness costs are the primary drivers of resistance patterns rather than intrinsic mutation rates. We observed three distinct growth patterns--delayed growth, two phase growth, and complete suppression--corresponding to specific parameter regimes as initial phage concentration increased. Two phase growth patterns emerged when competitive dynamics remained balanced, enabling coexistence of susceptible and resistant populations. Complete suppression patterns occurred when low proliferation thresholds combined with extreme competitive asymmetries created unsustainable conditions for resistant bacteria. These findings demonstrate that phage resistance evolution is fundamentally an ecological process where competitive context determines outcomes independently of mutation capacity, with important implications for phage therapy design.

evolutionary biology↗

bioRxiv2025

Defying Salinity, Drought, and pH Extremes: A Multifunctional Rhizobacterium, Burkholderia gladioli ST3M-39a, Matches Fertilizer Efficacy in Wheat via Phosphate Solubilization

Global phosphorus scarcity and the environmental impacts of chemical fertilizers necessitate sustainable microbial alternatives for agriculture. We characterized Burkholderia gladioli ST3M-39a, a maize rhizosphere isolate, as a multifunctional plant growth-promoting rhizobacterium with exceptional climate resilience. The strain achieved rapid phosphate solubilization (177.96 {+/-} 5.26 {micro}g/mL within 24 h; molybdenum-antimony assay), zinc solubilization, and ammonia production, EPS production, and produced stress-alleviating enzymes (cellulase and protease). Crucially, it maintained robust growth and phosphate-mobilizing capacity under extreme abiotic stresses: pH 4.5-8.5, 7.5% NaCl salinity, and drought-mimicking low water activity (aw 0.950, 32% sorbitol). In wheat trials, ST3M-39a inoculation significantly increased the growth parameters (p < 0.05 vs. those of the uninoculated controls), resulting in 85-92% of the biomass stimulation observed with diammonium phosphate (DAP) fertilizer. This multifunctional stress tolerance, coupled with its near-fertilizer efficacy, positioned ST3M-39a as a transformative bioinoculant for degraded soils. Field validation of its agricultural deployment and ecological impact is now pivotal.

microbiology↗

bioRxiv2025

Social stress worsens colitis through beta-adrenergic-driven oxidative stress in intestinal mucosal compartments

AbstractPsychological stress is a known risk factor for inflammatory bowel disease (IBD), but the mechanisms linking stress to worsened disease remain unclear. Because distinct stress paradigms activate different neuroimmune circuits, it is critical to investigate model-specific effects. We examined how social stress primes the gut for heightened inflammation and whether this is mediated by specific neuroendocrine pathways, including 2-/{beta}-adrenergic (sympathetic) or glucocorticoid/ corticotropin-releasing hormone receptor (CRHR1) (HPA axis) signaling. Mice were exposed to social disruption (SDR) stress and pre- treated with pharmacological antagonists targeting 2-adrenergic receptors (idazoxan), {beta}-adrenergic receptor ({beta}-AR) (propranolol), glucocorticoid receptor (mifepristone), or CRHR1 (antalarmin). Intestinal epithelial cell (IEC) gene expression and microbiota composition were assessed following SDR. To determine disease impact, SDR was combined with either Citrobacter rodentium infection or dextran sulfate sodium (DSS)-induced colitis, with interventions including the {beta}-AR inhibitor propranolol and the NADPH oxidase inhibitor apocynin. SDR significantly upregulated expression of Dual oxidase 2 (Duox2), Dual oxidase maturation factor 2 (Duoxa2), and inducible nitric oxide synthase 2 (Nos2) in IECs (2- to 8- fold, p < 0.0001), effects reversed by {beta}-AR blockade but not 2-adrenergic, CRH, or glucocorticoid inhibition. SDR also induced microbial dysbiosis, characterized by reduced alpha-diversity and compositional shifts, which was rescued by propranolol. Stress exacerbated disease severity in both infectious (C. rodentium) and chemically induced (DSS) colitis, amplifying colonic expression of Duox2, Nos2, and Ccl2, especially. Apocynin mitigated stress-induced ROS/RNS production and body weight loss even prior to colitis onset, reduced colonic gene expression of key oxidative enzymes, and alleviated both chemically and infectious colitis severity. These findings provide strong evidence that social stress sensitizes the gut to inflammation through {beta}-adrenergic and NADPH oxidase-driven oxidative stress, highlighting potential therapeutic targets for mitigating stress-exacerbated IBD. HighlightsSocial disruption (SDR) and restraint stress (RST) activate distinct neuroendocrine pathways, with SDR driving epithelial ROS/RNS pathways via {beta}-adrenergic signaling. {beta}-adrenergic blockade prevents SDR-induced epithelial priming, microbial dysbiosis, and colitis exacerbation. NADPH oxidase inhibition with apocynin mitigates stress-induced oxidative stress and disease severity across different colitis models. Findings identify {beta}-adrenergic and redox pathways as therapeutic targets for stress-exacerbated IBD.

immunology↗

bioRxiv2025

Estimation of stature from hand length and hand breadth in undergraduate medical students: An anthropometric study

BackgroundStature, a determinant that aids in personal identification, can be estimated using measurements of various body parts. This study measured the length and breadth of hands and the height of the participants, aiming to develop linear regression equations for stature estimation. MethodsThis is a cross-sectional descriptive study in which 195 medical students aged 18 to 24 were enrolled, and measurement of stature was done by stadiometer and hand length and breadth by vernier calliper, after an informed written consent was obtained. ResultsMean stature was higher in males (170.24{+/-}5.79 cm) as compared to females (159.01{+/-}7.261 cm). Mean length and breadth of both right and left hands were also found to be higher in males when compared with females. With a standard error of estimates of 5.083 cm and an R2 of 0.648, the multiple linear regression analysiss model summary concluded that R is .805, indicating a strong positive association between stature estimation and hand dimensions. ConclusionsHand length and hand breadth together may be a powerful predictor of stature, as indicated by the greater R value when compared to regression coefficients derived for other body parts. A variable entity, height is influenced by genetics and nutritional status. Future studies can be done taking these factors into consideration and also including a larger population size.

systems biology↗

bioRxiv2025

Genetic architecture and cellular basis of flag leaf size variation in barley

Flag leaf is the major contributor of photosynthetic assimilates to developing grains. We investigated the genetic architecture and cellular basis of flag leaf length (FLL) and width (FLW) in a multi-parent population comprised of 45 recombinant inbred line (RIL) populations (HvDRR) in barley. Fine mapping of a major quantitative trait locus (QTL) was performed as a first step to isolate the causal gene. Natural variation of FLL and FLW across multi-environment was highly heritable and genotypes adapted to warm climate produced longer and wider flag leaf than those adapted to cooler regions. The variation in flag leaf size was quantitatively inherited and influenced by 24 consensus QTLs of which 17 have not been reported earlier. Further, validation of QTL qHvDRR-FLS-8 and qHvDRR-FLS-17 in nearly isogenic RILs demonstrated that these QTLs also controlled length and width of leaves older than flag leaf. The number of epidermal cells primarily determined the differences in FLL and FLW. In addition, we identified the previously unknown effect of genic- and epiallele at Vrn-H1 on flag leaf size variation in spring barley. Furthermore, we fine-mapped qHvDRR-FLS-8, narrowing the interval from 8.7 to 3.5 Mb. In conclusion, our study identified the genomic regions associated with morphological and anatomical variation for leaf size and set the stage to uncover causal genes.

genetics↗

bioRxiv2025

Proteome-Wide Discovery of Degradable Proteins Using Bifunctional Molecules

Targeted protein degradation (TPD) is an emergent therapeutic strategy with the potential to circumvent challenges associated with targets unamenable to conventional pharmacological inhibition. Among TPD approaches, Proteolysis Targeting Chimeras (PROTACs) have shown marked advancement with numerous candidates in clinical development. Despite their potential, most PROTACs utilize advanced small molecule inhibitors, inherently limiting the scope of this approach. More generally, the fraction of the proteome tractable to PROTAC-type strategies is unknown. Here, we describe a chemical proteomic strategy for the agnostic discovery of degradable human proteins in cells using a new class of bifunctional degrader molecules called "AgnoTACs". Proteome-wide screening of 72 AgnoTACs in human cells uncovered downregulation events spanning >50 functionally and structurally diverse proteins, most of which lack chemical probes. Our findings highlight the potential of function-biased chemical libraries coupled with proteomic profiling to discover degrader starting points as well as furnish a blueprint for expanding our understanding of the chemically degradable proteome.

biochemistry↗

bioRxiv2025

Engineering Conjugative Plasmids for Inducible Horizontal DNA Transfer

Rapidly developing microbial resistance to existing antimicrobials poses a growing threat to public health and global food security. Current chemical-based treatments target cells by inhibiting growth or metabolic function, but their effectiveness is diminishing. To address the growing antimicrobial resistance crisis, there is an urgent need for innovative therapies. Conjugative plasmids, a natural mechanism of horizontal gene transfer in bacteria, have been repurposed to deliver toxic genetic cargo to recipient cells, showing promise as next-generation antimicrobial agents. However, the ecological risks posed by unintended gene transfer require robust biocontainment strategies. In this study, we developed inducible conjugative plasmids to solve these challenges. Utilizing an arabinose-inducible promoter, we evaluated 13 plasmids with single essential gene deletions, identifying trbC and trbF as strong candidates for stringent regulation. These plasmids demonstrated inducibility in both cis and trans configurations, with induction resulting in up to a 5-log increase in conjugation efficiency compared to uninduced conditions. Although challenges such as reduced conjugation efficiency and promoter leakiness persist, this work establishes a foundation for the controlled transfer of plasmids, paving the way for safer and more effective antimicrobial technologies.

synthetic biology↗

bioRxiv2025

Processing of Clostridium perfringens Enterotoxin by Intestinal Proteases

C. perfringens type F isolates are a leading cause of food poisoning and antibiotic-associated diarrhea. Type F isolate virulence requires production of C. perfringens enterotoxin [CPE], which acts by forming large pore complexes in host cell plasma membranes. During disease, CPE is produced in the intestines when type F strains undergo sporulation. The toxin is then released into the intestinal lumen when the mother cell lyses at the completion of sporulation. Once present in the lumen, CPE encounters intestinal proteases. This study examined in vitro, ex vivo and in vivo processing of CPE by intestinal proteases and the effects of this processing on CPE activity. Results using purified trypsin or mouse intestinal contents detected rapid cleavage of CPE to a major band of [~]32 kDa and studies with Caco-2 cells showed this processed CPE still forms large complexes and retains cytotoxic activity. When mouse small intestinal loops were challenged with CPE, the toxin caused intestinal histologic damage despite rapid proteolytic processing of most CPE to 32 kDa within 15 min. Intestinal large CPE complexes became more stable with longer treatment times. These results indicate that CPE processing involving trypsin occurs in the intestines and the processed toxin retains enterotoxicity.

microbiology↗

bioRxiv2024

Investigating the barley methylome, its variation and association with genomic, transcriptomic, and phenotypic variation

Epigenetic variation contributes to explaining the missing heritability of complex traits. In order to understand the genome-wide methylation variation in spring barley, our objectives were to gain fundamental insight into the barley methylome through whole genome bisulfite sequencing, characterizing methylation variation among 23 parental inbreds of a community resource for genetic mapping of phenotypic traits, and assessing the association of differentially methylated regions (DMRs) with single nucleotide polymorphisms (SNPs) and gene expression variation. Compared to other angiosperms, barley was found to have a highly methylated genome with an average genome wide methylation level of 88.6%, 58.1%, and 1.4% in the CpG, CHG, and CHH sequence context, respectively. We identified just below 500 000 differentially methylated regions (DMRs) among the inbreds. About 64%, 64%, and 83% of the DMRs were not associated with genomic variation in the CpG, CHG, and CHH context, respectively. The methylation level of around 6% of all DMRs was significantly associated with gene expression, where the directionality of the correlation was depended on the relative location of the DMR to the respective gene with a recognizable pattern. Notably, this pattern was much more specific and spatially confined than the association of methylation with gene expression across genes in a singular inbred line. We exemplified this association between DNA methylation and gene expression on the known flowering promoting gene VRN-H1 and identified a highly methylated epiallele associated with earlier flowering time. Finally, methylation was shown to improve the prediction abilities of genomic prediction models for a variety of traits over models using solely SNPs and gene expression as predictors. These observations highlight the independence of DNA methylation to sequence variation and their difference in information content. Our discoveries suggest that epigenetic variation provides a layer of information likely not predictable by other means and is therefore a valuable addition to genomic prediction models.

plant biology↗

bioRxiv2024

In situ deposition of nanobodies by an engineered commensal microbe promotes survival in a mouse model of enterohemorrhagic E. coli

Engineered smart microbes that deliver therapeutic payloads are emerging as treatment modalities, particularly for diseases with links to the gastrointestinal tract. Enterohemorrhagic E coli (EHEC) is a causative agent of potentially lethal hemolytic uremic syndrome. Given concerns that antibiotic treatment increases EHEC production of Shiga toxin (Stx), which is responsible for systemic disease, novel remedies are needed. EHEC encodes a type III secretion system (T3SS) that injects Tir into enterocytes. Tir inserts into the host cell membrane, exposing an extracellular domain that subsequently binds intimin, one of its outer membrane proteins, triggering the formation of attaching and effacing (A/E) lesions that promote EHEC mucosal colonization. Citrobacter rodentium (Cr), a natural A/E mouse pathogen, similarly requires Tir and intimin for its pathogenesis. Mice infected with Cr({Phi}Stx2dact), a variant lysogenized with an EHEC-derived phage that produces Stx2dact, develop intestinal A/E lesions and toxin-dependent disease. Stx2a is more closely associated with human disease. By developing an efficient approach to seamlessly modify the C. rodentium genome, we generated Cr_Tir-MEHEC({Phi}Stx2a), a variant that expresses Stx2a and the EHEC extracellular Tir domain. We found that mouse pre-colonization with HS-PROT3EcT-TD4, a human commensal E. coli strain (E. coli HS) engineered to efficiently secrete- an anti-EHEC Tir nanobody, delayed bacterial colonization and improved survival after challenge with Cr_Tir-MEHEC({Phi}Stx2a). This study provides the first evidence to support the efficacy of engineered commensal E. coli to intestinally deliver therapeutic payloads that block essential enteric pathogen virulence determinants, a strategy that may serve as an antibiotic-independent antibacterial therapeutic modality. Significance StatementEngineered smart microbes that secrete therapeutics are emerging as treatment modalities, particularly for gut-based diseases. With the growing threat of multidrug-resistant infection, non-antibiotic treatments are urgently needed. The gastrointestinal pathogen enterohemorrhagic E coli (EHEC) can cause the potentially lethal hemolytic uremic syndrome, a toxin-driven disease. Given concerns that antibiotics increase toxin release, treatment is largely limited to supportive care. Here, we show that pre-treatment with a commensal E. coli (HS-PROT3EcT) engineered to secrete an antibody that blocks an essential EHEC virulence factor delays the establishment of an EHEC-like infection in mice. This study strongly suggests that smart microbes that deliver payloads that block colonization factors of gut pathogens can be developed as critically needed alternatives to antibiotics for fighting bacterial infections.

microbiology↗

bioRxiv2024

Morphological, physiological and metabolic responses of diverse barley inbreds to dry down and moderate drought stress

Drought stress alters the metabolic activity, physiological processes, and plant growth and such responses might differ with the intensity of stress. We evaluated the genotypic diversity on plant morphology, photosynthetic responses, metabolite shift and their relationship in diverse barley inbreds under dry down (DD) and moderate drought (MD) stress using 23 genetically diverse parental inbreds of genetic mapping population of barley. MD stress caused a strong growth reduction, while DD stress triggered inhibition of photosynthetic health. We observed that the induced changes occurred in a genotype-dependent manner. Compared to control conditions, the metabolism of simple sugars and polyhydroxy acids increased in MD and DD, while the maximum accumulation of amino acid, lipids and phosphates occurred in DD stress. Accumulation of hexose and metabolites with unknown classification was the metabolic signature of drought tolerant inbreds. The inbreds tolerant to MD originated from the temperate regions while those tolerant to both MD and DD came from semi-arid regions. Low stomata density, reduced water loss and retarded growth under drought stress were the key features of inbreds with better survival capacity under severe dehydration. We identified drought tolerant barley inbreds and our study offers resources for future genetic research on various drought tolerance strategies.

plant biology↗

bioRxiv2024

Aging amplifies a gut microbiota immunogenic signature linked to heightened inflammation

Aging is associated with low-grade inflammation that increases the risk of infection and disease, yet the underlying mechanisms remain unclear. Gut microbiota composition shifts with age, harboring microbes with varied immunogenic capacities. We hypothesized the gut microbiota acts as an active driver of low-grade inflammation during aging. Microbiome patterns in aged mice strongly associated with signs of bacterial-induced barrier disruption and immune infiltration, including marked increased levels of circulating lipopolysaccharide (LPS)-binding protein (LBP) and colonic calprotectin. Ex vivo immunogenicity assays revealed that both colonic contents and mucosa of aged mice harbored increased capacity to activate toll-like receptor 4 (TLR4) whereas TLR5 signaling was unchanged. We found patterns of elevated innate inflammatory signaling (colonic Il6, Tnf, Tlr4) and endotoxemia (circulating LBP) in young germ-free mice after 4 weeks of colonization with intestinal contents from aged mice compared with young counterparts, thus providing a direct link between aging-induced shifts in microbiota immunogenicity and host inflammation. Additionally, we discovered that the gut microbiota of aged mice exhibited unique responses to a broad-spectrum antibiotic challenge (Abx), with sustained elevation in Escherichia (Proteobacteria) and altered TLR5 immunogenicity 7 days post-Abx cessation. Together, these data indicate that old age results in a gut microbiota that differentially acts on TLR signaling pathways of the innate immune system. We found that these age-associated microbiota immunogenic signatures are less resilient to challenge and strongly linked to host inflammatory status. Gut microbiota immunogenic signatures should be thus considered as critical factors in mediating chronic inflammatory diseases disproportionally impacting older populations.

immunology↗

bioRxiv2023

Do native and introduced cover crops differ in their ability to suppress weeds and reduce seedbanks? A Case study in a Table Grape Vineyard.

Cover cropping is considered a valuable tool for integrated weed management. However, weed suppression by cover crops can be inconsistent. We hypothesized that a native cover crop species may have greater capacity to suppress weeds than an introduced species owing to adaptive advantages. A study was conducted from 2020 to 2022 in a newly-established Autumn King tablegrape vineyard in Parlier, CA. Two cover crop treatments, a native plant species, phacelia (Phacelia tanacetifolia), or an introduced species, rye (Secale cereale L. Merced), were compared to a no cover crop, herbicide-managed control for impacts on weed control. Cover crops were sown in 2019 in the center 1.8 m of the 3.6 m space between the grapevine rows. The experimental design was a randomized complete block with four replications. Percent cover, weed density, and weed biomass in different seasons were assessed in the inter-row spaces and the vine rows. Soil samples were collected in 2021 from the grape row and interrow spaces to assess the weed seedbank. After the cover crops were terminated, percent weed cover was lower in the interrow of the phacelia compared to the no cover crop plots at two sampling times. When cover crops were actively growing (winter/spring), phacelia plots had a 7-fold higher cover crop to weed biomass ratio compared to that of the rye plots, thus indicating greater weed suppression. However, weed seedling emergence from the seedbank samples of the cover crop plots were 2- to 4-fold greater (in the phacelia and rye, respectively) than from the no cover crop plots. In summary, phacelia suppressed weeds more than rye; however, they both resulted in a bigger weed seedbank size compared to the herbicide-managed no cover crop plots, so additional management practices will be needed for long term weed management with cover crops in vineyards.

ecology↗