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Whether the heat and cold tolerance of endotherms evolve independently or correlatively remains unresolved. Both physiological trade-offs and natural selection can contribute to a coevolutionary pattern of heat and cold tolerance in endotherms. Using a published database, we tested the correlation between upper and lower thermal limits across endothermic species with multi-response generalized linear mixed models incorporating phylogenies. We found a positive correlation between upper and lower thermal limits, which suggested a coevolutionary pattern of heat and cold tolerance. Specifically, this relationship between heat and cold tolerance is phylogenetically constrained for tropical endotherms but not for temperate endotherms. The correlated evolution between heat and cold tolerance may have a significant influence on endotherms' evolution and ecology and needs to be further investigated. [ABSTRACT FROM AUTHOR]

Wildlife can be viewed as a renewable resource at ecologically viable levels, but illicit consumption is a major threat to global biodiversity. Using data from crime cases is an emerging new tool for assessing the motives and drivers of wildlife offenders. This approach can be used with behavior change frameworks to devise more effective conservation strategies. We used data from 20,145 online judgments published between 2014 and 2019 to determine the spatial distribution of different wildlife crime and illegal consumption patterns across China, and used multiscale modeling to test the effects of socioeconomic, geographic, and demographic correlates. The results indicated that geographic indicators and agricultural practices had a broad and positive impact on wildlife consumption, implying wildlife availability was a powerful incentive for wildlife crimes. In addition, urbanization and industrial structure were regionally sensitive in predicting convictions for wild meat, traditional medicine, and human-nature conflicts. Given the socioeconomic transformation in modern China, we predict that functional approaches of wildlife utilization will decrease in the coming years, but the illegal consumption characterized by financial and spiritual demand is unlikely to diminish. As a response, the prevention strategy should strengthen law enforcement on non-functional consumption and enhance nature education campaigns among youths across the country. [ABSTRACT FROM AUTHOR]

Non‐linear immune response is one of the causes of multi‐stability of infection outcomes. In order to avoid the uncertainty caused by multi‐stability in experiments, one needs to quantitatively measure immune response and other traits as well. Here, we took a quantitative approach, which combines mathematical model and time‐series data, to measure the immune response of the Tenebrio moliter challenged by non‐replicative immune inducers. The results showed that the host immunity that characterized by in‐vitro bacterial killing rapidly mounted after immune challenging, then slowly declined to an undetectable level within 100 h. We then quantified the immunity at 15 h after challenging. The results showed that immune response was non‐linearly correlated with the titter of inducer, which fits well to a Hill‐like function. Our results have verified the non‐linear immune response with respect to amount of invading pathogens and may also help to rigorously test the concepts and theories in host–pathogen interaction, such as resistance and tolerance. [ABSTRACT FROM AUTHOR]

Background: Previous studies have shown that the vitrification of metaphase II (MII) oocytes significantly represses their developmental potential. Abnormally increased oxidative stress is the probable factor; however, the underlying mechanism remains unclear. The walnut-derived peptide TW-7 was initially isolated and purified from walnut protein hydrolysate. Accumulating evidences implied that TW-7 was a powerful antioxidant, while its prospective application in oocyte cryopreservation has not been reported. Result: Here, we found that parthenogenetic activation (PA) zygotes derived from vitrified MII oocytes showed elevated ROS level and delayed progression of pronucleus formation. Addition of 25 μmol/L TW-7 in warming, recovery, PA, and embryo culture medium could alleviate oxidative stress in PA zygotes from vitrified mouse MII oocytes, furtherly increase proteins related to histone lactylation such as LDHA, LDHB, and EP300 and finally improve histone lactylation in PA zygotes. The elevated histone lactylation facilitated the expression of minor zygotic genome activation (ZGA) genes and preimplantation embryo development. Conclusions: Our findings revealed the mechanism of oxidative stress inducing repressed development of PA embryos from vitrified mouse MII oocytes and found a potent and easy-obtained short peptide that could significantly rescue the decreased developmental potential of vitrified oocytes, which would potentially contribute to reproductive medicine, animal protection, and breeding. [ABSTRACT FROM AUTHOR]

Genetic engineering using negative regulators of plant immunity has the potential to provide a huge impetus in agricultural biotechnology to achieve a higher degree of disease resistance without reducing yield. Type 2C protein phosphatases (PP2Cs) represent the largest group of protein phosphatases in plants, with a high potential for negative regulatory functions by blocking the transmission of defence signals through dephosphorylation. Here, we established a PP2C functional protoplast screen using pFRK1::luciferase as a reporter and found that 14 of 56 PP2Cs significantly inhibited the immune response induced by flg22. To verify the reliability of the system, a previously reported MAPK3/4/6‐interacting protein phosphatase, PP2C5, was used; it was confirmed to be a negative regulator of PAMP‐triggered immunity (PTI). We further identified PP2C15 as an interacting partner of BRI1‐associated receptor kinase 1 (BAK1), which is the most well‐known co‐receptor of plasma membrane‐localized pattern recognition receptors (PRRs), and a central component of PTI. PP2C15 dephosphorylates BAK1 and negatively regulates BAK1‐mediated PTI responses such as MAPK3/4/6 activation, defence gene expression, reactive oxygen species bursts, stomatal immunity, callose deposition, and pathogen resistance. Although plant growth and 1000‐seed weight of pp2c15 mutants were reduced compared to those of wild‐type plants, pp2c5 mutants did not show any adverse effects. Thus, our findings strengthen the understanding of the mechanism by which PP2C family members negatively regulate plant immunity at multiple levels and indicate a possible approach to enhance plant resistance by eliminating specific PP2Cs without affecting plant growth and yield. [ABSTRACT FROM AUTHOR]

Dysfunctions of the ovaries and adrenal glands are both evidenced to cause aberrant adipose tissue (AT) remodeling and resultant metabolic disorders, but their distinct and common roles are poorly understood. In this study, through biochemical, histological and RNA-seq analyses, we comprehensively explored the mechanisms underpinning subcutaneous (SAT) and visceral adipose tissue (VAT) remodeling, in response to ovariectomy (OVX) versus adrenalectomy (ADX) in female mice. OVX promoted adipocyte differentiation and fat accumulation in both SAT and VAT, by potentiating the Pparg signaling, while ADX universally prevented the cell proliferation and extracellular matrix organization in both SAT and VAT, likely by inactivating the Nr3c1 signaling, thus causing lipoatrophy in females. ADX, but not OVX, exerted great effects on the intrinsic difference between SAT and VAT. Specifically, ADX reversed a large cluster of genes differentially expressed between SAT and VAT, by activating 12 key transcription factors, and thereby caused senescent cell accumulation, massive B cell infiltration and the development of selective inflammatory response in SAT. Commonly, both OVX and ADX enhance circadian rhythmicity in VAT, and impair cell proliferation, neurogenesis, tissue morphogenesis, as well as extracellular matrix organization in SAT, thus causing dysfunction of adipose tissues and concomitant metabolic disorders. [ABSTRACT FROM AUTHOR]

As all insect GH1 genes originate from a common ancestor based on the gene phylogeny, duplications and losses of the insect GH1 gene family are likely associated with insect adaptations to the insect-plant interactions. However, a systematic evolutionary analysis of GH1 genes spanning various insect orders is lacking, hindering our understanding of the role of GH1 genes in insect adaptations to plant utilization. Along with the diverse enzyme activities of insect GH1s, the evolution of the GH1 gene family provides further insights into our understanding of insect-plant interactions. The one copy of the GH1 gene inferred in the ancestor of insects indicates the gain of functions in GH1 genes during insect evolution. [Extracted from the article]

Background: Salivary gland (SMG) degeneration and dysfunction are common symptoms that occur after sex hormone deprivation, but the underlying mechanisms remain largely unknown. Additionally, immunocastration, which causes drop of sex hormones, has been developed as an alternative to surgical castration, however whether it exerts similar effects as surgical castration on the salivary glands is unknown. Through histological and RNA-seq analysis, we assessed changes in morphology and transcriptome of SMG in response to immunocastration (IM) versus surgical castration (bilateral orchiectomy, ORC). Results: Compared to entire males (EM), ORC caused severe degeneration of SMG in rats, as evidenced by both decreased (P < 0.01) SMG weight and organ index, and by decreased (P < 0.01) quantity of SMG acini and ducts. IM had minimal effects (P > 0.05) on SMG weight and organ index, but it still caused degeneration (P < 0.05) of the acini and ducts. Even though, the quantity of both SMG acini and ducts was much higher (P < 0.001) in IM than in ORC. Functional enrichment analysis of the common regulated genes by ORC/IM revealed disrupted epithelial cell development, angiogenesis, anatomical structure morphogenesis and enhanced cell death are associated with SMG degeneration in deprivation of androgens. Integrated data analysis shown that there existed a selective hyperfunction of SMG ribosome and mitochondrion in ORC but not in IM, which might be associated with more severe degeneration of SMG in ORC than in IM. Conclusions: Our findings suggested that both surgical castration and immunocastration caused SMG degeneration by disrupting epithelial cell development, angiogenesis, anatomical structure morphogenesis and enhancing cell death. But, surgical castration selectively induced hyperfunction of SMG ribosome and mitochondrion, thus causing more severe degeneration of SMG than immunocastration. [ABSTRACT FROM AUTHOR]

Follicle-stimulating hormone (FSH) has been newly demonstrated to play a great role in promoting fat accumulation, providing a potential to target FSH for controlling fat accumulation and treating obesity. A short, 13-amino acid of FSHβ (FSHβ13AA) was indentified to be the FSH receptor-binding epitope in both humans and mice. By conservation analysis, we found such FSHβ13AA is highly conserved across species. Accordingly, we designed a new FSH antigen by synthesizing a tandem of FSHβ13AA (LVYKDPARPNIQK) and then conjugating it to ovalbumin (FSHβ13AA-T-OVA). Then, we tested its efficacy in suppressing fat accumulation in both ovariectomized and intact mouse models. Vaccination with this novel antigen emulsified in mild adjuvant, Specol, was highly effective in preventing ovariectomy-induced body weight gain and fat accumulation in mice (P < 0.01). Mechanistically, FSH vaccination treatment inhibited lipid biosynthesis by inactivating PPARγ adipogenic signaling pathway and simultaneously enhanced adipocyte themogenesis via upregulating UCP1 expression in both visceral and subcutaneous adipose tissues. Moreover, injection of this novel FSH vaccine also substantially reduced (P < 0.05) fat accumulation in both intact male and female mice. These actions result from the specific binding of the generated antibody to the β-subunit to block its action, rather than lowering the circulating levels of FSH, as evidenced by nearly no alterations in serum FSH levels in mice following FSH vaccination. Overall, we developed a novel FSH antigen and vaccine, and demonstrated it is highly efficacious in suppressing fat accumulation. • A novel FSH vaccine was developed based on the FSH receptor-binding epitope of FSH β-subunit. • Vaccination with this vaccine was highly effective in preventing ovariectomy-induced fat accumulation in mice. • Vaccination with this vaccine was also highly effective in preventing fat accumulation in intact mice fed on normal chow. • FSH vaccination suppresses fat accumulation through inactivating PPARγ and upregulating UCP1 signaling in adipose tissues. [ABSTRACT FROM AUTHOR]

Lipopolysaccharide (LPS) is a classical pathogen-associated molecular pattern that can trigger strong inflammatory response mainly by TLR4-mediated signaling pathway in mammals, but the molecular mechanism of anti-LPS immunity is unclear in teleost fishes. In this study, we analyzed the gene expression features based on transcriptome analysis in Schizothorax prenanti (S. prenanti), after stimulation with two sources of LPS from Aeromonas hydrophila and Escherichia coli (Ah. LPS and Ecoli. LPS). 921 different expression genes (DEGs) after Ah. LPS stimulation and 975 DEGs after Ecoli. LPS stimulation were acquired, but only 706 and 750 DEGs were successfully annotated into the databases, respectively. Both of two groups of DGEs were significantly enriched into immune-related pathways by KEGG enrichment analysis, such as "Toll-like receptor signaling pathway", "Cytokine-cytokine receptor interaction" and "JAK-STAT signaling pathway". The annotated DEGs from Ah. LPS and Ecoli. LPS stimulation shared 470 DEGs, including 88 immune-related DEGs (IRGs) identified mainly by KEGG enrichment to immune-related signaling pathways. Among the shared IRGs, four pattern-recognition genes (TLR5 , TLR25 , PTX3 and C1q) were induced with high expression foldchange, and IFN-γ and relative genes also showed higher expression levels than control. Meanwhile, inflammatory signals were highlighted by upregulating the expression of inflammatory cytokines (IL-1β , IL-10 and IL-8). Moreover, some non-shared IRGs (including TLR2 and TLR4) were identified, suggesting that different sources of LPS own different potentials for the induction of immune gene expression. In conclusion, TLR5, TLR25, PTX3 and C1q may function as the sensing molecules to catch the invasion signal of LPS. The anti-LPS immune response may be involved into TLR25/TLR5-mediated inflammatory signals that regulate subsequently the activation of PTX3/C1q-modulated complement pathway upon the induction of PTX3 expression, and the crosstalk between IFN-γ and TLR signaling pathways in teleost fishes. This study will contribute to further explore the molecular mechanism of LPS-induced immunity in teleost fishes. • 921 different expression genes (DEGs) after Ah. LPS stimulation and 975 DEGs after Ecoli. LPS stimulation were acquired. • The stimulation with Ah. LPS and Ecoli. LPS shared 470 DEGs including 88 immune-related DEGs (IRGs). • TLR5, TLR25, PTX3 and C1q were predicted as the potential pattern-recognition molecules in LPS sensing. • IFN-γ-mediated signaling pathway may play an important role in protecting teleost fishes against LPS. [ABSTRACT FROM AUTHOR]

Mammal Toll-like receptor 5 (TLR5) can directly recognize bacterial flagellin, initiate the inflammatory signaling cascades and trigger body immune system to clear the "non-self" substances. In teleosts, TLR5 has presented more complexes not only in increasing the molecular types, but also in elevating the functional diversity. In this study, we identified two TLR5 family members in Schizothorax prenanti , named as spTLR5-1 and spTLR5-2. The complete coding sequence (CDS) of spTLR5-1 is 2622 bp, encoding 873 amino acids, while the complete CDS of spTLR5-2 is 2640 bp, encoding 879 amino acids. Phylogenetic analysis showed that spTLR5-1 and spTLR5-2 were clustered to the TLR5 of schizothorax richardsonii and Cyprinus carpio respectively. The 3D structure analysis exhibited that the α-helix, β-sheet, and the ligand binding site of spTLR5-1, spTLR5-2 and human TLR5 have large differences. The spTLR5-1 and spTLR5-2 had extensively expressed in various tissues, including the higher expression in liver, spleen and head kidney. Both the expression levels of spTLR5-1 and spTLR5-2 were significantly up-regulated after Aeromonas hydrophila (A. hydrophila) challenge. And, the downstream genes, such as AP-1 , IKK-α , NF-kB , IL-1β , IL-8 and TNF-α , were also significantly up-regulated after A. hydrophila challenge. Apart from that, the luciferase reporter assay demonstrated that the co-transfection of spTLR5-1 or spTLR5-2 into HEK293T cells showed the significantly increased NF-kB luciferase activity after flagellin stimulation. In conclusion, our results reveal that both two molecular types of fish TLR5 may commonly mediate the recognition of flagellin and the activation of the downstream inflammatory signaling molecules. • spTLR5-1 and spTLR5-2 have similar structures and localize on the cell membrane. • Both spTLR5-1 and spTLR5-2 could respond to Aeromonas hydrophila challenge. • Both spTLR5-1 and spTLR5-2 could significantly activated NF-κB signaling pathway upon flagellin stimulation. [ABSTRACT FROM AUTHOR]

Evolutionary development has increased the diversity of genotypes and the complexity of gene functions in fish. TLR2 2 has been identified as a teleost-specific gene, but its functions are tremendously different among different fish species. Whether the functional diversity relates to the difference of genotypes remains poorly understand. In this study, we cloned and identified three TLR22 molecules from Schizothorax prenanti (S. prenanti), named as spTLR22-1 , spTLR22-2 and spTLR22-3. The full-length coding regions of spTLR22s are 2841 bp, 2805 bp and 2868 bp and coding 946 aa, 934 aa and 955 aa, respectively. All spTLR22s are composed of multiple leucine-rich repeat (LRR) domains, a transmembrane structure and a Toll/IL-1 receptor (TIR) region. The phylogenetic analysis showed that three spTLR22s were close to Cyprinus carpio TLR22-1, TLR22-2 and TLR22-3, respectively. Among the spTLR22s, they presented not close relationship but remained to belong to TLR22 subfamily. All spTLR22s were ubiquitously expressed in all tested tissues, but the expression levels of spTLR22s were dominant in immune-related tissues, such as gill and spleen. The expression levels of spTLR22-1 and spTLR22-3 were significantly increased after treatment with bacteria, LPS and Poly(I:C). However, spTLR22-2 seems like no response to these treatments. The luciferase reporter assay demonstrated that all spTLR22s could activate NF-κB signaling pathway, but only spTLR22-1 and spTLR22-2 could activate IFN-β signaling pathway. Interestingly, in the ligand recognition analysis, spTLR22-1 and spTLR22-3 but not spTLR22-2 had the recognized potential to Poly(I:C), and all spTLR22s could not recognize LPS. Both spTLR22-1 and spTLR22-3 significantly up-regulated the expression of anti-viral-related genes (Mx , IFN and ISG15) and down-regulated the expression of anti-inflammatory factor IL-10 after the overexpression in carp EPC cell line, but spTLR22-2 failed to impact the expression of these genes. Moreover, we found that all spTLR22s localized to the intracellular region. Taken together, our results reveal that spTLR22-1 and spTLR22-3 but not spTLR22–2 may be involved into the anti-viral immune response via IFN-β signaling pathway, and all spTLR22s can activate NF-κB signaling pathway but only spTLR22-1 and spTLR22-3 response to the stimulation of bacteria and LPS. • Both spTLR22-1 and spTLR22-3 but not spTLR22-2 positively responded to bacteria, LPS and Poly(I:C) stimulation. • All the spTLR22s could activate NF-κB-mediated signaling pathway, but only spTLR22-1 and spTLR22-2 could activate IFN-β-mediated signaling pathway. • Both spTLR22-1 and spTLR22-3 had the recognized potential to Poly(I:C), but all the spTLR22s did not show the interaction with LPS. [ABSTRACT FROM AUTHOR]

A novel hybrid manufacturing method of arc-directed energy deposition (ADED) + rotary friction processing (RFP) was developed herein to eliminate the porosity defects of ADED high-strength aluminum alloys. To understand the mechanism of pore elimination, the morphology evolution of pores in hybrid-manufactured ER2319 aluminum alloy was quantitatively studied, and the grain structures, dislocations, and nano-precipitates of manufactured metals were characterized. The results showed that the pores in ADED aluminum alloy significantly compressed and closed during RFP. After RFP with a 3.4-kN peak load, the porosity area fraction and roundness level were decreased by 71.8 % and 35.7 %, respectively, improving the ADED densification ratio by more than 99 %. RFP led to grain breaking and the dynamic reversion and recrystallization of deposited metals. The elimination mechanism of the closed pores was mainly attributed to the growth and connection of sub-grains. Further, the diffusible [H] that dissociated from the molecular hydrogen of deforming pores could be captured by high-density dislocations, high-angle grain boundaries, and nano-precipitates. Due to the porosity reduction and grain refinement, the horizontal and vertical tensile strengths of hybrid manufactured ER2319 aluminum alloy were respectively improved by 6 % and 12 % after heat treatment, reaching 456.2 and 454.8 MPa, respectively, and mechanical anisotropy was eliminated. [ABSTRACT FROM AUTHOR]

Many pattern-recognition receptors (PRRs) and their corresponding ligands have been identified. However, it is largely unknown how similar and different these ligands are in inducing plant innate immunity and affecting plant development. In this study, we examined three well characterized ligands in Arabidopsis thaliana , namely flagellin 22 (flg22), plant elicitor peptide 1 (pep1) and a conserved 20-amino-acid fragment found in most necrosis and ethylene-inducing peptide 1-like proteins (nlp20). Our quantitative analyses detected the differences in amplitude in the early immune responses of these ligands, with nlp20-induced responses typically being slower than those mediated by flg22 and pep1. RNA sequencing showed the shared differentially expressed genes (DEGs) was mostly enriched in defense response, whereas nlp20-regulated genes represent only a fraction of those genes differentially regulated by flg22 and pep1. The three elicitors all inhibited primary root growth, especially pep1, which inhibited both auxin transport and signaling pathway. In addition, pep1 significantly inhibited the cell division and genes involved in cell cycle. Compared with flg22 and nlp20, pep1 induced much stronger expression of its receptor in roots, suggesting a potential positive feedback regulation in the activation of immune response. Despite PRRs and their co-receptor BAK1 were necessary for both PAMP induced immune response and root growth inhibition, bik1 mutant only showed impaired defense response but relatively normal root growth inhibition, suggesting BIK1 acts differently in these two biological processes. • In this study, flg22, pep1 and nlp20 , three PAMP/DAMP elicitors from different sources were selected to explore the conservation and divergence of immune response and inhibition of root development, which results highlighted that (1) flg22 is more effective in Arabidopsis leaves, whereas pep1 boost the expression of its receptor leading to stronger responses in roots; (2) pep1 integrated hormone, cell division, cell cycle and development signals to inhibit root growth; (3) Elicitors treated bik1 mutant showed similar root growth inhibition but decreased ROS burst, suggesting that regulation of root inhibition might be different from that of immune response. [ABSTRACT FROM AUTHOR]

Toll-like receptor 18 (TLR18), a non-mammalian TLR, has been believed to play an important role in anti-bacterial immunity of teleost fishes. UNC93B1 is a classical molecular chaperone that mediates TLRs transport from endoplasmic reticulum to the located membrane. However, TLR18-mediated signal transduction mechanism and the regulatory effect of UNC93B1 to TLR18 are still unclear in teleost fishes. In this study, the coding sequences of TLR18 and UNC93B1 were cloned from Schizothorax prenanti , named spTLR18 and spUNC93B1 , respectively. The spTLR18 and spUNC93B1 are 2583 bp and 1878 bp in length, encode 860 and 625 amino acids, respectively. The spTLR18 widely expressed in various tissues with the highest expression level in liver. After stimulation of Aeromonas hydrophila , lipopolysaccharide (LPS) and Poly(I:C), the expression levels of spTLR18 were significantly increased in spleen and head kidney. The spTLR18 located in the cell membrane, while spUNC93B1 located in the cytoplasm. Luciferase and overexpression analysis showed that spTLR18 activated NF-κB and type I IFN signal pathways, and spTLR18-mediated NF-κB activation might depend on the adaptor molecule MyD88. Besides, spUNC93B1 positively regulates spTLR18-mediated NF-κB signal. Our study first uncovers TLR18-UNC93B1-mediated signal transduction mechanism, which contributes to the understanding of TLR signaling pathway in teleost fishes. [Display omitted] • SpTLR18 responses to stimulation of LPS, Poly(I:C) and Aeromonas hydrophila in spleen and head kidney. • SpTLR18 may activate NF-κB and type I IFN signal pathways. • SpTLR18 may activate NF-κB via MyD88-dependent pathway. • SpUNC93B1 positively regulates spTLR18-mediated NF-κB signal. [ABSTRACT FROM AUTHOR]

The nucleotide-binding oligomerization domain 2 (NOD2) has been identified as an important sensor for microorganic invasion in both mammals and teleost fishes. In this study, two splicing variants of NOD2 (NOD2-v1 and NOD2-v2) were identified as truncating the functional domains of wild-type NOD2 in the teleost fish Schizothorax prenanti. NOD2-v1 included an intron sequence that terminated within the third leucine-rich repeat (LRR) domain, while NOD2-v2 incorporated an insertion of one and half intron sequences and truncated within the second caspase activation and recruitment domain (CARD). NOD2 , NOD2-v1 and NOD2-v2 genes were ubiquitously expressed. All three genes positively responded to exposure of Aeromonas hydrophila and lipopolysaccharide stimulation in varying degrees. Using luciferase activity assays in HEK293T cells, our results revealed that NOD2 activated the NF-κB signal and recognized muramyl dipeptide (MDP). NOD2-v1 exhibited deficiency in the LRR domains and could not sense MDP, but maintained the ability to activate NF-κB and enhanced NOD2-mediated MDP recognition. Given the significant change to the functional structure, NOD2-v2 lost its capacity for NF-κB activation, but interestingly repressed NOD2-mediated MDP sensing and NF-κB activation, and even NOD2-v1-induced NF-κB activation. Altogether, our study reveals a novel pattern of signal regulation by splicing variants in teleost fishes. • Human-like NOD2 splicing variants were firstly identified in S. prenanti , named NOD2, NOD2-v1 and NOD2-v2. • NOD2 and NOD2-v1 but NOD2-v2 can induce NF-κB activation. • NOD2-v1 and NOD2-v2 lose the function of sensing specific ligand MDP. • NOD2-v2 represses NOD2-mediated MDP sensing and NF-κB activation, and even NOD2-v1-induced NF-κB activation. [ABSTRACT FROM AUTHOR]

Bacillus spp. are the dominant spoilage organisms in a rehydrated non-fermented soy product, Sichuan yuba in China. In this study, we used two spoilage Bacillus amyloliquefaciens strains DY1a and DY1b to evaluate their destructive capability on rehydrated Sichuan yuba at 25 °C. Compared with the uninoculated soy product, the texture profile of the inoculated samples showed that the hardness, springiness, chewiness, and cohesiveness decreased significantly. Scanning electron microscope (SEM) revealed that the surface of bacteria-inoculated soy product was scattered with deep holes and loose film network structure. The subsequent analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) indicated that the α and α' subunit of 7S globulin and the acid subunit of 11S glycinin were hydrolyzed by Bacillus during storage. In addition, disulfide bond contents in inoculated samples decreased by 38.7–27.5%. Protein secondary structure characterized using Fourier transform infrared spectroscopy (FTIR) revealed that spoilage Bacillus inoculation reduced the β-sheet by 13.02–14.11%, and increased the β-turn by 15.55–16.00%. Consequently, the texture deterioration of Sichuan yuba was associated with soy protein degradation caused by B. amyloliquefaciens. • Textures and protein changes of rehydrated Sichuan yuba inoculated with spoilage Bacillus were analyzed. • B. amyloliquefaciens could hydrolyze the α and α′ subunit of 7S and the acidic subunit of 11S. • B. amyloliquefaciens changed molecular interactions and the secondary structure of soy protein. • Protein degradation by B. amyloliquefaciens contributed to the texture deterioration of rehydrated Sichuan yuba. [ABSTRACT FROM AUTHOR]