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Genome-wide identification of the superoxide dismutase gene family in Lycium barbarum and their expression profiles under abiotic stress and phytohormone treatment.

BACKGROUND: Superoxide dismutases (SODs) are crucial metalloenzymes that constitute the first line of defense against reactive oxygen species in plants under abiotic stress. Wolfberry (Lycium barbarum) is an economically important medicinal plant with notable stress tolerance, however, a comprehensive genome-wide analysis of its SOD gene family has not yet been performed. RESULTS: We identified ten wolfberry SOD genes (LbaSODs) and classified them into three subfamilies: iron-SODs (Fe-SODs), manganese-SODs (Mn-SODs), and copper/zinc-SODs (Cu/Zn-SODs). Members within each subfamily shared conserved gene structures and motifs. Segmental duplication was the primary driver of LbaSOD expansion, with three paralogous pairs identified. Analysis of cis-regulatory elements in the promoter region revealed a predominance of stress- and hormone-responsive cis-elements, particularly ABA-responsive elements (ABREs) (22 copies) and LTR (17 copies) motifs. Tissue-specific expression profiling revealed that LbaSOD2 and LbaSOD5 expression peaked during early fruit development, whereas LbaSOD6, LbaSOD9, and LbaSOD10 were progressively upregulated through fruit maturation. Under abiotic conditions, Fe-SOD members were markedly suppressed during prolonged drought, whereas LbaSOD9 and LbaSOD10 were rapidly induced in response to salt stress. Among the phytohormone treatments, methyl jasmonate (MeJA) elicited the most pronounced response, with LbaSOD5 expression increasing by approximately 60-fold after 24 hours. Notably, abscisic acid (ABA) triggered an exceptionally strong transcriptional induction of LbaSOD5 (2.5 × 105-fold), LbaSOD10 (6 × 105-fold), and LbaSOD6 (70-fold). In addition, LbaSOD3 and LbaSOD7 transcripts were undetectable in any of the tested conditions. CONCLUSIONS: This study provides the first comprehensive characterization of the LbaSOD gene family and elucidates its hormone- and stress-responsive regulatory landscape, providing a valuable foundation for future functional investigations of LbaSOD genes in abiotic stress adaptation. The extraordinarily strong ABA-mediated induction of specific LbaSOD members, together with their tissue- and stress-specific expression patterns, highlights their potential as targets for genetic improvement of stress tolerance in wolfberry.

Lycium barbarum↗

Systematic mining and characterization of metal transporter families regulating zinc homeostasis provide insights into metal homeostasis in Camellia sinensis.

BACKGROUND AND AIMS: Zinc is essential for tea plant growth and quality formation, yet its homeostatic mechanisms remain poorly understood. This study identified metal transporter families regulating zinc homeostasis, analyzed their evolution, structure, and expression, and clarified zinc uptake, transport, detoxification networks, and their links to metabolism. METHODS: This study identified zinc homeostasis-related metal transporter families in the tea plant genome, characterized their structural features and expression profiles across tissues and developmental stages through integrative bioinformatics and transcriptomic analyses, and delineated the molecular mechanisms underlying zinc uptake, translocation, and detoxification by systematically integrating published evidence. RESULTS: This study identified 74 metal transporter genes from six families: 13 CsZIPs, 12 CsNRAMPs, 10 CsHMAs, 10 CsYSLs, 14 CsMTPs, and 15 CsCAXs in the 'Shuchazao2' genome, revealing closer affinity to woody species than to Arabidopsis. These proteins exhibit conserved domains, diverse subcellular localizations (cell membrane, vacuole, chloroplast, and Golgi apparatus), and tissue-specific expression with abundant stress/hormone-responsive cis-elements. At the plant-soil interface, tea plants mobilize rhizospheric zinc via proton and organic acid secretion; CsYSLs, CsNRAMPs, and CsZIPs mediate zinc uptake, aided by arbuscular mycorrhizal fungi (AMF) and plant growth-promoting rhizobacteria (PGPR) that expand root absorption zones. Xylem CsHMAs and phloem CsYSLs coordinate root-to-shoot zinc translocation, and vacuolar transporters (CsMTPs, CsCAXs), cell wall immobilization, and antioxidant systems alleviate high-zinc stress injury. CONCLUSIONS: These findings collectively delineate an integrated zinc "acquisition-distribution-buffering" network in tea plants, offering a repertoire of candidate genes with potential utility in zinc biofortification breeding and improving acid soil adaptation. Further experimental validation, including tea transgenesis, zinc-stress qRT-PCR, and heterologous functional complementation, is essential to substantiate their biological roles.

Camellia sinensis↗

Shared Genetic Architecture Between Atopic Dermatitis and Autoimmune Diseases.

Atopic dermatitis (AD) and autoimmune diseases exhibit epidemiological comorbidity, yet the shared genetic architecture remains incompletely understood. We investigated the genetic overlap between AD and three autoimmune disorders including inflammatory bowel disease (IBD), rheumatoid arthritis (RA), and vitiligo, leveraging genome-wide association data. Despite modest evidence for global genetic correlations, we found 113 independent pleiotropic loci shared among AD and autoimmune diseases, with 11 displaying a concordant effect across all 3 pairwise comparisons. Gene-set and tissue enrichment analyses evidenced the inflammatory background of pleiotropic associations. Multi-trait colocalization analysis prioritized 22 loci, linking the tissue-specific expression of DOK2, GPR132, RERE, RERE-AS1, SUOX, TNFRSF11A, and TRAF1 pleiotropic genes with AD risk. Mendelian randomization revealed no causal effect of genetic liability to AD on autoimmune diseases. Nevertheless, genetic liability to IBD increased AD risk, while vitiligo exhibited a protective effect post outlier correction. Our findings provide mechanistic insights into the multimorbidity of atopic dermatitis (AD) and autoimmune diseases, offering additional evidence for the pleiotropic genetic architecture of AD that contributes to systemic immune dysregulation across multiple organ systems.

Humans↗

Cucurbitacins in Plant-Insect Interactions: Biosynthesis, Regulation, Ecological Functions, and Prospects for Crop Protection.

Cucurbitacins are highly oxygenated tetracyclic triterpenoids characterized by intense bitterness, substantial structural diversity, and important consequences for plant-herbivore interactions. Although best known from Cucurbitaceae, cucurbitacins and related cucurbitane-type metabolites also occur in phylogenetically distant herbaceous and woody plants. Genetic and biochemical studies have validated several core biosynthetic steps, including cucurbitadienol formation by oxidosqualene cyclases and subsequent modification by cytochrome P450 monooxygenases, acyltransferases, and glycosyltransferases. Tissue-preferential basic helix-loop-helix transcription factors constitute the best-characterized regulatory layer, whereas the evidence supporting accessory regulators, transporters, and environmental responses varies from functional validation to transcriptomic or genomic prediction. From the plant perspective, cucurbitacins deter feeding or impair performance in many generalist and non-adapted herbivores. By contrast, their use as host-recognition cues and feeding stimulants by specialist diabroticite beetles reflects evolved herbivore adaptations involving perception, tolerance, metabolism, or sequestration rather than a second defensive function of the plant trait. Herbivore-induced cucurbitacin accumulation has been demonstrated in particular systems, although its regulatory mechanisms and ecological generality remain unresolved. Unlike previous reviews centered primarily on cucurbitacin chemistry, pharmacological activity, or individual biosynthetic pathways, this review integrates evidence-graded pathway reconstruction and molecular regulation with taxonomic distribution, insect adaptation, domestication, and agroecological consequences. Mechanistically, this review traces how scaffold formation, oxidative tailoring, conjugation, tissue-specific regulation, and transport give rise to contrasting ecological outcomes through herbivore-specific perception, tolerance, metabolism, and sequestration. We conclude that uniformly increasing or eliminating cucurbitacins is unlikely to provide broadly effective crop resistance because either direction may favor a different herbivore group. Future priorities include functional validation of candidate genes, spatially resolved metabolite analysis, comparative investigation of non-cucurbit lineages, and field evaluation involving generalist and specialist herbivores, crop quality, and non-target organisms. These advances will support context-specific fruit-quality improvement, behavioral pest control, and integrated pest management strategies rather than cucurbitacin manipulation as a stand-alone resistance approach.

agroecology↗

Genome-Wide Identification of the Soybean GH5 Gene Family and Functional Analysis of GmGH5-22 in Salt Tolerance.

Plant GH5 family genes function in both cell wall biosynthesis and stress responses. However, comprehensive studies on GH5 genes in the soybean remain limited. Here, we identified 28 GmGH5 genes from the soybean genome. Phylogenetic analysis assigned these genes to three subfamilies (I-III), with no representatives in subfamily IV. The GmGH5 family harbors 15 conserved motifs, which are largely similar within subfamilies but differ across subfamilies. Additionally, exon-intron structures (2-7 introns) exhibit clade-specific patterns, with members within the same clade sharing similar intron numbers and lengths, whereas distinct clades show some variation. The promoter regions of GmGH5 genes contained various cis-acting regulatory elements associated with stress responses and developmental processes. Transcriptome-based expression profiling revealed distinct tissue-specific expression patterns of GmGH5 genes. RT-qPCR further confirmed their differential expression under salt, alkaline, cold, and drought stresses, especially a significant increase in GmGH5-22 expression under salt stress (approximately 22-fold at 6 h, **** p < 0.0001). Furthermore, GmGH5-22 was highly expressed in roots, and transient expression in tobacco leaves showed its peripheral localization, which aligns with its predicted extracellular localization, suggesting that GmGH5-22 is highly likely localized to the cell wall. Overexpression of GmGH5-22 in soybean hairy roots significantly improved tolerance to salt stress. These findings establish a foundation for functional characterization of GmGH5 genes and provide viable targets for molecular breeding to enhance salt tolerance in soybeans.

GH5 family↗

The Key Trichoderma-Induced Gene Encoding a DUF568 Domain-Containing Protein Mediates Defense Responses in Wheat.

Genes encoding DUF568 domain-containing proteins participate in plant stress adaptation. To elucidate the functional role of DUF568 domain-containing genes in Trichoderma-induced wheat defense responses against wheat Fusarium crown rot, we performed a genome-wide identification and characterization of the TaDUF568 gene family in hexaploid wheat (Triticum aestivum L.). In this study, a total of 33 TaDUF568 family genes were systematically identified and characterized at the genome-wide level, exhibiting uneven chromosomal distribution and diverse physicochemical properties. Phylogenetic, structural, and collinearity analyses revealed conserved family characteristics among monocot species. Segmental duplication was verified as the primary driver of gene family expansion. Expression profiling revealed divergent tissue-specific expression patterns among TaDUF568 family members, among which TaDUF568.18 was strongly induced by Trichoderma M2. Subcellular localization assays confirmed that TaDUF568.18 is a plasma membrane-localized protein. Functional validation via stable transgenes demonstrated that overexpression of TaDUF568.18 restricted lesion expansion, improved agronomic traits, and enhanced disease resistance. This study is the first to characterize the wheat DUF568 family and confirm that TaDUF568.18 (annotated as TaAIR12) acts as a positive regulator of Trichoderma-mediated wheat defense, providing a valuable gene resource for wheat disease-resistance breeding.

DUF568↗

Clinical Variant Interpretation with the Integrative Genomics Viewer (IGV) for Molecular Pathologists.

The integrative genomics viewer (IGV) is a pivotal tool in clinical genomics, enabling the visualization and interpretation of complex sequencing data. Bringing clinical knowledge to bear with visual evaluation of sequencing results is the primary means by which molecular pathologists and other professionals assess and finalize cases. A variety of software tools can assist, but their relationship to the underlying data must be understood and applied systematically. This study includes essential background on next-generation sequencing (NGS) data file types (e.g., FASTQ, BAM, VCF) with a discussion of their format and purpose. We then describe features of IGV that derive nuances from these files. We utilize a series of curated practical cases based on clinical vignettes through which the reader will interact with clinical NGS sequencing data using the IGV software to review various types of clinically relevant variants relative to the human reference genome. These clinical vignettes have been curated to describe examples of some of the complexities of interpretation of genomic data, and how utilizing IGV as part of a routine workflow can provide additional interpretive information for variants beyond routine bioinformatic software algorithm variant calls. The visual inspection of genomic variants utilizing the tools within IGV can unmask subtle contextual cues (i.e., variant allele frequency, strand bias, tissue-specific context) that can influence the interpretation of genomic variants. Although this study focuses on using IGV for the detection and interpretation of somatic variants, the provided applications can be extrapolated for use in the germline setting, including analysis of complex variants and detection of mosaicism.

Humans↗

Genetic evidence prioritizes circulating proteins for heart failure beyond shared BMI-related genetic liability.

BACKGROUND: Heart failure (HF) and body mass index (BMI) share substantial genetic architecture, which may lead genetically informed target discovery to preferentially identify adiposity-related pathways. We sought to identify circulating proteins associated with HF beyond this shared genetic component. METHODS: We applied GWAS-by-subtraction to overall HF, nonischemic HF, and nonischemic HF with reduced or preserved ejection fraction to derive BMI-related and BMI-subtracted HF components. We then performed proteome-wide cis-pQTL Mendelian randomization and colocalization using four independent proteomic cohorts, followed by tissue-specific eQTL colocalization, cardiac transcriptomic annotation, and druggability assessment. RESULTS: Compared with the original HF phenotypes, the BMI-subtracted components showed attenuated genetic correlations with BMI (0.045-0.147) while retaining 28 independent loci for overall HF and nine for nonischemic HF. Across 19,930 protein-HF tests, 11 associations involving nine proteins were prioritized by the Mendelian randomization and colocalization analyses. For example, a 1-SD increase in genetically predicted CELSR2 abundance was associated with lower overall HF risk (odds ratio, 0.96 [95% CI, 0.94-0.98]; P=8.6&#xd7;10-7), whereas a 1-SD increase in genetically predicted CSF3 abundance was associated with higher nonischemic HF risk (odds ratio, 1.32 [95% CI, 1.18-1.48]; P=2.0&#xd7;10-6). CELSR2 and TMEM106B colocalized with cis-eQTLs in failing left ventricular myocardium, and DAG1 showed cardiomyocyte enrichment with concordant downregulation in failing hearts. CONCLUSIONS: We identified nine circulating proteins associated with HF beyond the genetic component shared with BMI. These findings extend the range of genetically supported pathways implicated in HF and nominate candidate proteins for further mechanistic and therapeutic investigation.

Genetics↗

Red blood cell selection in chimeric mice.

Starch gel electrophoresis of a large number of tissues and organs from C3H in equilibrium C57BL aggregation chimeras suggests that the C57BL red blood cell population predominates, whereas for other tissues the proportions of the two components are more nearly equal. A similar predominance of (C57BL X C3H)F1 red blood cells is seen in (C57BL X C3H)F1 in equilibrium Recessive chimeras. Analysis of blood samples taken from the same animals at different times suggests that a temporal shift in the proportions of the two component red cell populations occurs in some adult chimeras and results in an unbalanced chimeric phenotype. It is suggested that differential mitotic activity contributes to strain-dependent, tissue-specific selection pressures in the erythropoietic tissue.

Age Factors↗

Immunogenetic factors in preeclampsia and eclampsia. Erythrocyte, histocompatibility, and Y-dependent antigens.

Determination of ABO and HL-A antigens and sex ratio of infants born to 46 women with preeclampsia or eclampsia, in comparison with normal controls, disclosed no predominant blood group, HL-A haplotype, or qualitative difference in maternal-fetal incompatibility. These results suggest that a link between immunologic mechanisms and the pathogenesis of toxemia syndromes, if present at all, must be associated with feto-placental tissue-specific antigens.

ABO Blood-Group System↗

Immunospecificity of non-histone chromosomal proteins in 89Sr-induced osteogenic sarcoma (mouse).

Antibodies against non-histone chromosomal proteins for 89Sr-induced osteogenic sarcoma (mouse) were prepared by immunization of rabbits. The immunoreactivity of this antigen was then compared with those of non-histone chromosomal proteins from Ehrlich ascites tumor, normal mouse liver, and calf thymus by the method of quantitative microcomplement fixation. The non-histone chromosomal proteins of 98Sr-induced osteogenic sarcoma, fractionated by hydroxylapatite chromatography, exhibited significant affinity for the antibodies. Similar proteins from Ehrlich ascites tumor, normal mouse liver, or calf thymus were virtually inactive, indicating the tissue-specificity of 89Sr-induced osteogenic sarcoma proteins.

Animals↗

[Thermostable antigens of malignant tumors and normal tissues of experimental animals].

Gel precipitation and immunoelectrophoresis tests tests demonstrated the presence of thermostable antigens in dimethylbenzanthracene-induced malignant tumours of the muscle tissues of Wistar rats. These antigens were relatively tissue-specific for the tumours, amniotic fluid and the uterus on the one hand, and for the lung, spleen, and the serum on the other hand. The thermostable antigens of the tumours and the amniotic fluid had the electrophoretic mobility in the zone of alpha and alpha1-globulins.

9,10-Dimethyl-1,2-benzanthracene↗

[Tissue specific antigen of the caudal lobe of the chicken adenohypophysis].

The tissue-specific water-soluble antigen of the chick pituitary gland was revealed by immunochemical analysis. The content of this antigen was found to be predominant in the caudal lobe of the adenohypophysis. The antigen was found from the 13th day of embryogenesis by immunoelectrophoresis and immunofluorescence. Two kinds of the antigen (with high and low relative electrophoretic mobility) were discovered in the chick adenohypophysis. A conclusion was drawn that the adenohypophysis cells differed by the differentiation level.

Age Factors↗

[Immunohistochemical study of the differentiation of the cephalic lobe of the adenohypophysis in chick embryos].

It was shown by means of indirect immunofluorescence that ACTH appeared in the cephalic lobe of the chick embryo pituitary beginning from the 8th day of the development. A new tissue-specific antigen (A3) is revealed, which is localized in the cephalic lobe of adenohypophysis and becomes manifest at the 7th day of embryogenesis. Quantitative analysis of ACTH and A3 localization in the cells of 11-day chick embryo adenohypophyses allows a conclusion that A3 is localized in corticotropic cells.

Adrenocorticotropic Hormone↗

Purification of a human prostate specific antigen.

Rabbit antiserum raised against the crude extract of normal human prostatic tissue contained antibodies to a prostatic tissue-specific antigen as shown by immunoprecipitation techniques. Using this antiserum a prostate antigen was detected in normal, benign hypertrophic, and malignant prostatic tissues, but not in other human tissues. The prostate antigen was purified to homogeneity from prostatic tissues and showed a single protein band on analytical polyacrylamide gel electrophoresis and isoelectric focusing. This report thus presents the first demonstration of the purification of a prostate-specific antigen that does not represent prostatic acid phosphatase.

Antigens↗

[Immunopathogenesis of the Vogt-Koyanagi-Harada syndrome].

Regarding immunopathogenesis of the Vogt-Koyanagi-Harada syndrome (VKHS), peripheral blood lymphocytes of a female patient with this disease were tested for sensitization against several antigens such as myelinic basic protein (BP) and uveoretinal, brain and spleen tissue homogenates. For comparison, cells of seven patients with chorioretinitis only and cells of six patients with encephalitis of unknown etiology were also tested. Cells of healthy donors served as controls. The electromobility test and the leucocyte migration test were used as in vitro test systems for cell-mediated immunological reactivity. The results show a strong sensitivity against BP and uveoretinal and brain tissue homogenates in VKHS. In the patients suffering from chorioretinitis, a strong reactivity against uveoretinal homogenate only was found, while in patients with encephalitis, responses to brain antigens only were observed. Reactions towards spleen tissue homogenate were negative in all experiments. The extent to which this tissue-specific immunological reactivity, which is different from the monoreactivity in chorioretinitis or encephalitis, might be a characteristic phenomenon of the VKHS is discussed.

Eye Proteins↗

[Antitumor resistance induced by immunization with normal definitive tissues].

Immunization of C3HA mice with homogenates of various normal definitive tissues, obtained from syngeneic, allogeneic and xenogeneic donors, resulted in an increase of antitumor resistance, as evidenced by a considerable retardation of growth of the transplantable strain-specific hepatoma 22a. The effect may be due to sensibilization of animals to the antigens of normal definitive cells, and, in particular to the tissue-specific antigens characteristic of cells of the tumor in question.

Animals↗

TNF-NF-&#x3ba;B signaling mediates immune-biomineralization crosstalk during shell repair under ocean acidification in Mytilus edulis.

Ocean acidification (OA) impairs biomineralization in bivalves, but its effects on immune-biomineralization crosstalk during shell repair remain unknown. Here, we exposed adult Mytilus edulis bearing standardized shell perforations to three pH levels (8.1, 7.9, and 7.7) for up to 40 days. OA slowed early repair and caused microstructural disorganization and an approximately 87% reduction of compressive strength at pH 7.7, yet the damaged area appeared largely closed by day 15, suggesting a decoupling between morphological closure and functional recovery. In addition, transcriptomic profiling of hemocytes and mantle tissue, based on an average of 6.5&#x202f;Gb of clean reads per sample mapped to the M. edulis reference genome (NCBI Assembly GCF_000511035.1), revealed that these shell-level defects were accompanied by coordinated immune and metabolic reprogramming. Hemocytes, the primary immune effector cells of bivalves, exhibited pH- and time-dependent shifts with moderate acidification (pH 7.9) promoting inflammatory transcripts, whereas severe acidification (pH 7.7) suppressed these signals while upregulating stress-associated pathways; both treatments consistently downregulated lysosomal proteases and NF-&#x3ba;B negative regulators. The mantle, a primarily mineralizing organ, paradoxically upregulated immune-related genes while suppressing oxidative phosphorylation and extracellular matrix pathways. This tissue-level imbalance, with hemocytes recruited but functionally constrained and mantle metabolically suppressed yet immunologically activated, points to TNF-NF-&#x3ba;B pathway modulation as a key mediator of shell repair under acidification. Our findings demonstrate that visible shell closure masks underlying structural and mechanical failure, and that immune regulation, rather than simple suppression or activation, critically shapes the repair outcome. These results advocate for multifunctional indicators beyond closure area to assess shell integrity in acidified marine environments.

Animals↗