Tuning Apoptosis and Neuroinflammation: TBK1 Restrains RIPK1.

Partial loss of TANK-binding kinase 1 (TBK1) causes amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Xu et al. identify the role of TBK1 in suppressing neuroinflammation and apoptosis by its inhibition of the receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and elucidate how aging and genetic susceptibility together cause neuroinflammation.

Allosteric activation of functionally asymmetric RAF kinase dimers.

Although RAF kinases are critical for controlling cell growth, their mechanism of activation is incompletely understood. Recently, dimerization was shown to be important for activation. Here we show that the dimer is functionally asymmetric with one kinase functioning as an activator to stimulate activity of the partner, receiver kinase. The activator kinase did not require kinase activity but did require N-terminal phosphorylation that functioned allosterically to induce cis-autophosphorylation of the receiver kinase. Based on modeling of the hydrophobic spine assembly, we also engineered a constitutively active mutant that was independent of Ras, dimerization, and activation-loop phosphorylation. As N-terminal phosphorylation of BRAF is constitutive, BRAF initially functions to activate CRAF. N-terminal phosphorylation of CRAF was dependent on MEK, suggesting a feedback mechanism and explaining a key difference between BRAF and CRAF. Our work illuminates distinct steps in RAF activation that function to assemble the active conformation of the RAF kinase.

The strigolactone receptor DWARF14 regulates flowering time in Arabidopsis.

Multiple plant hormones, including strigolactone (SL), play key roles in regulating flowering time. The Arabidopsis (Arabidopsis thaliana) DWARF14 (AtD14) receptor perceives SL and recruits F-box protein MORE AXILLARY GROWTH2 (MAX2) and the SUPPRESSOR OF MAX2-LIKE (SMXL) family proteins. These interactions lead to the degradation of the SMXL repressor proteins, thereby regulating shoot branching, leaf shape, and other developmental processes. However, the molecular mechanism by which SL regulates plant flowering remains elusive. Here, we demonstrate that intact strigolactone biosynthesis and signaling pathways are essential for normal flowering in Arabidopsis. Loss-of-function mutants in both SL biosynthesis (max3) and signaling (Atd14 and max2) pathways display earlier flowering, whereas the repressor triple mutant smxl6/7/8 (s678) exhibits the opposite phenotype. Retention of AtD14 in the cytoplasm leads to its inability to repress flowering. Moreover, we show that nuclear-localized AtD14 employs dual strategies to enhance the function of the AP2 transcription factor TARGET OF EAT1 (TOE1). AtD14 directly binds to TOE1 in an SL-dependent manner and stabilizes it. In addition, AtD14-mediated degradation of SMXL7 releases TOE1 from the repressor protein, allowing it to bind to and inhibit the FLOWERING LOCUS T (FT) promoter. This results in reduced FT transcription and delayed flowering. In summary, AtD14 perception of SL enables the transcription factor TOE1 to repress flowering, providing insights into hormonal control of plant flowering.

Hydrogen Embrittlement as a Conspicuous Material Challenge─Comprehensive Review and Future Directions.

Hydrogen is considered a clean and efficient energy carrier crucial for shaping the net-zero future. Large-scale production, transportation, storage, and use of green hydrogen are expected to be undertaken in the coming decades. As the smallest element in the universe, however, hydrogen can adsorb on, diffuse into, and interact with many metallic materials, degrading their mechanical properties. This multifaceted phenomenon is generically categorized as hydrogen embrittlement (HE). HE is one of the most complex material problems that arises as an outcome of the intricate interplay across specific spatial and temporal scales between the mechanical driving force and the material resistance fingerprinted by the microstructures and subsequently weakened by the presence of hydrogen. Based on recent developments in the field as well as our collective understanding, this Review is devoted to treating HE as a whole and providing a constructive and systematic discussion on hydrogen entry, diffusion, trapping, hydrogen-microstructure interaction mechanisms, and consequences of HE in steels, nickel alloys, and aluminum alloys used for energy transport and storage. HE in emerging material systems, such as high entropy alloys and additively manufactured materials, is also discussed. Priority has been particularly given to these less understood aspects. Combining perspectives of materials chemistry, materials science, mechanics, and artificial intelligence, this Review aspires to present a comprehensive and impartial viewpoint on the existing knowledge and conclude with our forecasts of various paths forward meant to fuel the exploration of future research regarding hydrogen-induced material challenges.

Combined analysis of the effects of hypoxia and oxidative stress on DNA methylation and the transcriptome in HTR-8/SVneo trophoblast cells.

The alterations in DNA methylation and transcriptome in trophoblast cells under conditions of low oxygen and oxidative stress have major implications for pregnancy-related disorders. However, the exact mechanism is still not fully understood. In this study, we established models of hypoxia (H group) and oxidative stress (HR group) using HTR-8/SVneo trophoblast cells and performed combined analysis of genome-wide DNA methylation changes using reduced representation bisulphite sequencing and transcriptome expression changes using RNA sequencing. Our findings revealed that the H group exhibited a higher number of differentially methylated genes and differentially expressed genes than the HR group. In the H group, only 0.90% of all differentially expressed genes displayed simultaneous changes in DNA methylation and transcriptome expression. After the threshold was expanded, this number increased to 6.29% in the HR group. Notably, both the H group and HR group exhibited concurrent alterations in DNA methylation and transcriptome expression within Axon guidance and MAPK signalling pathway. Among the top 25 differentially methylated KEGG pathways in the promoter region, 11 pathways were commonly enriched in H group and HR group, accounting for 44.00%. Among the top 25 KEGG pathways in transcriptome with significant differences between the H group and HR group, 10 pathways were consistent, accounting for 40.00%. By integrating our previous data on DNA methylation from preeclamptic placental tissues, we identified that the ANKRD37 and PFKFB3 genes may contribute to the pathogenesis of preeclampsia through DNA methylation-mediated transcriptome expression under hypoxic conditions.

CK1δ/ε kinases regulate TDP-43 phosphorylation and are therapeutic targets for ALS-related TDP-43 hyperphosphorylation.

Hyperphosphorylated TAR DNA-binding protein 43 (TDP-43) aggregates in the cytoplasm of neurons is the neuropathological hallmark of amyotrophic lateral sclerosis (ALS) and a group of neurodegenerative diseases collectively referred to as TDP-43 proteinopathies that includes frontotemporal dementia, Alzheimer's disease, and limbic onset age-related TDP-43 encephalopathy. The mechanism of TDP-43 phosphorylation is poorly understood. Previously we reported casein kinase 1 epsilon gene (CSNK1E gene encoding CK1ε protein) as being tightly correlated with phosphorylated TDP-43 (pTDP-43) pathology. Here we pursued studies to investigate in cellular models and in vitro how CK1ε and CK1δ (a closely related family sub-member) mediate TDP-43 phosphorylation in disease. We first validated the binding interaction between TDP-43 and either CK1δ and CK1ε using kinase activity assays and predictive bioinformatic database. We utilized novel inducible cellular models that generated translocated phosphorylated TDP-43 (pTDP-43) and cytoplasmic aggregation. Reducing CK1 kinase activity with siRNA or small molecule chemical inhibitors resulted in significant reduction of pTDP-43, in both soluble and insoluble protein fractions. We also established CK1δ and CK1ε are the primary kinases that phosphorylate TDP-43 compared to CK2α, CDC7, ERK1/2, p38α/MAPK14, and TTBK1, other identified kinases that have been implicated in TDP-43 phosphorylation. Throughout our studies, we were careful to examine both the soluble and insoluble TDP-43 protein fractions, the critical protein fractions related to protein aggregation diseases. These results identify CK1s as critical kinases involved in TDP-43 hyperphosphorylation and aggregation in cellular models and in vitro, and in turn are potential therapeutic targets by way of CK1δ/ε inhibitors.

Artificial Intelligence in battling infectious diseases: A transformative role.

It is widely acknowledged that infectious diseases have wrought immense havoc on human society, being regarded as adversaries from which humanity cannot elude. In recent years, the advancement of Artificial Intelligence (AI) technology has ushered in a revolutionary era in the realm of infectious disease prevention and control. This evolution encompasses early warning of outbreaks, contact tracing, infection diagnosis, drug discovery, and the facilitation of drug design, alongside other facets of epidemic management. This article presents an overview of the utilization of AI systems in the field of infectious diseases, with a specific focus on their role during the COVID-19 pandemic. The article also highlights the contemporary challenges that AI confronts within this domain and posits strategies for their mitigation. There exists an imperative to further harness the potential applications of AI across multiple domains to augment its capacity in effectively addressing future disease outbreaks.

Integrated self-injection-locked narrow linewidth laser based on thin-film lithium niobate.

Narrow linewidth lasers have a wide range of applications in the fields of coherent optical communications, atomic clocks, and measurement. Lithium niobate material possesses excellent electro-optic and thermo-optic properties, making it an ideal photonic integration platform for a new generation. The light source is a crucial element in large-scale photonic integration. Therefore, it is essential to develop integrated narrow linewidth lasers based on low-loss LNOI. This study is based on the multimode race-track type add-drop microring resonator with multimode interferometric coupler (MMRA-MRR) of the DFB laser self-injection-locked, to achieve the narrowing of linewidth to the laser. The microring external cavity was used to narrow the linewidth of the laser to 2.5 kHz. The output power of the laser is 3.18 mW, and the side-mode suppression ratio is 60 dB. This paper presents an integrated low-noise, narrow-linewidth laser based on thin-film lithium niobate material for the communication band. This is significant for achieving all-optical device on-chip integration of lithium niobate material in the future. It has great potential for use in high-speed coherent optical communication.

Upregulation of Phosphodiesterase 7A Contributes to Concurrent Pain and Depression via Inhibition of cAMP-PKA-CREB-BDNF Signaling and Neuroinflammation in the Hippocampus of Mice.

BACKGROUND: Phosphodiesterases (PDEs) are enzymes that catalyze the hydrolysis of cyclic adenosine monophosphate AMP (cAMP) and/or cyclic guanosine monophosphate (cGMP). PDE inhibitors can mitigate chronic pain and depression when these disorders occur individually; however, there is limited understanding of their role in concurrent chronic pain and depression. We aimed to evaluate the mechanisms of action of PDE using 2 mouse models of concurrent chronic pain and depression. METHODS: C57BL/6J mice were subjected to partial sciatic nerve ligation (PSNL) to induce chronic neuropathic pain or injected with complete Freund's adjuvant (CFA) to induce inflammatory pain, and both animals showed depression-like behavior. First, we determined the change in PDE expression in both animal models. Next, we determined the effect of PDE7 inhibitor BRL50481 or hippocampal PDE7A knockdown on PSNL- or CFA-induced chronic pain and depression-like behavior. We also investigated the role of cAMP-protein kinase A (PKA)-cAMP response element binding protein (CREB)-brain-derived neurotrophic factor (BDNF) signaling and neuroinflammation in the effect of PDE7A inhibition on PSNL- or CFA-induced chronic pain and depression-like behavior. RESULTS: This induction of chronic pain and depression in the 2 animal models upregulated hippocampal PDE7A. Oral administration of PDE7 inhibitor, BRL50481, or hippocampal PDE7A knockdown significantly reduced mechanical hypersensitivity and depression-like behavior. Hippocampal PDE7 inhibition reversed PSNL- or CFA-induced downregulation of cAMP and BDNF and the phosphorylation of PKA, CREB, and p65. cAMP agonist forskolin reversed these changes and caused milder behavioral symptoms of pain and depression. BRL50481 reversed neuroinflammation in the hippocampus in PSNL mice. CONCLUSIONS: Hippocampal PDE7A mediated concurrent chronic pain and depression in both mouse models by inhibiting cAMP-PKA-CREB-BDNF signaling. Inhibiting PDE7A or activating cAMP-PKA-CREB-BDNF signaling are potential strategies to treat concurrent chronic pain and depression.

Glycolytic enzyme PGK1 promotes M1 macrophage polarization and induces pyroptosis of acute lung injury via regulation of NLRP3.

Acute lung injury (ALI) is characterized by an unregulated inflammatory reaction, often leading to severe morbidity and ultimately death. Excessive inflammation caused by M1 macrophage polarization and pyroptosis has been revealed to have a critical role in ALI. Recent study suggests that glycolytic reprogramming is important in the regulation of macrophage polarization and pyroptosis. However, the particular processes underlying ALI have yet to be identified. In this study, we established a Lipopolysaccharide(LPS)-induced ALI model and demonstrated that blocking glycolysis by using 2-Deoxy-D-glucose(2-DG) significantly downregulated the expression of M1 macrophage markers and pyroptosis-related genes, which was consistent with the in vitro results. Furthermore, our research has revealed that Phosphoglycerate Kinase 1(PGK1), an essential enzyme in the glycolysis pathway, interacts with NOD-, LRR- and pyrin domain-containing protein 3(NLRP3). We discovered that LPS stimulation improves the combination of PGK1 and NLRP3 both in vivo and in vitro. Interestingly, the absence of PGK1 reduces the phosphorylation level of NLRP3. Based on in vitro studies with mice bone marrow-derived macrophages (BMDMs), we further confirmed that siPGK1 plays a protective role by inhibiting macrophage pyroptosis and M1 macrophage polarization. The PGK1 inhibitor NG52 suppresses the occurrence of excessive inflammation in ALI. In general, it is plausible to consider a therapeutic strategy that focuses on modulating the relationship between PGK1 and NLRP3 as a means to mitigate the activation of inflammatory macrophages in ALI.

Allelic phenotype prediction of phenylketonuria based on the machine learning method.

BACKGROUND: Phenylketonuria (PKU) is caused by mutations in the phenylalanine hydroxylase (PAH) gene. Our study aimed to predict the phenotype using the allelic genotype. METHODS: A total of 1291 PKU patients with 623 various variants were used as the training dataset for predicting allelic phenotypes. We designed a common machine learning framework to predict allelic genotypes associated with the phenotype. RESULTS: We identified 235 different mutations and 623 various allelic genotypes. The features extracted from the structure of mutations and graph properties of the PKU network to predict the phenotype of PKU were named PPML (PKU phenotype predicted by machine learning). The phenotype of PKU was classified into three different categories: classical PKU (cPKU), mild PKU (mPKU) and mild hyperphenylalaninemia (MHP). Three hub nodes (c.728G>A for cPKU, c.721 for mPKU and c.158G>A for HPA) were used as each classification center, and 5 node attributes were extracted from the network graph for machine learning training features. The area under the ROC curve was AUC = 0.832 for cPKU, AUC = 0.678 for mPKU and AUC = 0.874 for MHP. This suggests that PPML is a powerful method to predict allelic phenotypes in PKU and can be used for genetic counseling of PKU families. CONCLUSIONS: The web version of PPML predicts PKU allele classification supported by applicable real cases and prediction results. It is an online database that can be used for PKU phenotype prediction http://www.bioinfogenetics.info/PPML/ .

Unraveling Ice-Solid Interface Rupture Dynamics: Insights from Molecular Dynamics Simulations.

Unwanted icing on exposed surfaces poses significant risks, driving the quest for effective anti-icing mechanisms. While fracture mechanics concepts have been developed for designing coatings that weaken the ice-solid interface on soft surfaces, the factors that dictate ice adhesion strength and its counterpart, ice removal force, on hard surfaces remain poorly understood. In this study, we employ molecular dynamics simulations to investigate the interface rupture between ice and a hard solid substrate. The results indicate that the ice adhesion strength is contingent on the length of the ice cube. By examining the shearing behavior, we reveal a nanoscale critical force-bearing length. The shear force required to detach the ice scales proportionally with the length of the ice cube when it is smaller than the critical length. Once the ice cube length exceeds the critical length, the shear force stabilizes at a constant maximum value, revealing the existence of a maximum ice-removal force. The results align with the so-called strength versus toughness-controlled deicing regimes and are in agreement with cohesive zone modeling at the continuum length scale and recent experimental results. Our results extend this understanding to the nanoscale, confirming consistency between macro and micro scales. This consistency suggests that the toughness of the ice-solid interface is intrinsically governed by ice-surface interactions. By unraveling key intrinsic factors and their scale-dependent effects on the interface rupture of ice on surfaces, this study lays a solid theoretical foundation for the design and fabrication of next-generation anti-icing surfaces.

Role of ASC, a key component of the inflammasome in the antimicrobial process in black rockfish (Sebastes schlegelii).

Apoptosis-associated speck-like protein containing a CARD (ASC) serves as a pivotal component within the inflammasome complex, playing a critical role in the activation of the innate immune response against pathogenic infection. However, the functional significance of inflammasome ASC in teleosts remains unclear. In this study, the coding sequence (CDS) region of ASC gene of Sebastes schlegelii (SsASC) was cloned, and we observed a high conservation of SsASC with teleosts through comprehensive bioinformatics analysis. SsASC and SsCaspase-1 were found to be highly expressed in immune tissues such as spleen and head kidney. Furthermore, our findings revealed that SsASC interacts with SsCaspase-1 through CARD-CARD interactions to generate oligomeric speck-like structures, whereas the PYD structural domain of SsASC forms only filamentous structures. To further understand the role of SsASC in combating Edwardsiella piscicida (E. piscicida) infection, we developed a SsASC knockdown model using in vivo siRNA injection and E. piscicida challenge via intraperitoneal injection. The model demonstrated that E. piscicida infection up-regulated SsASC expression, which was markedly reduced upon SsASC knockdown. Concurrently, E. piscicida colonization was significantly enhanced in the knockdown group, accompanied by a suppression of inflammatory factor expression. These findings confirm the pivotal antibacterial and anti-infective role of SsASC in the Sebastes schlegelii immune response upon E. piscicida stimulation. Our study highlights the significance of SsASC in the innate immune defense mechanism of teleosts against bacterial pathogens.

C-type lectin 12B/4E of black rockfish (Sebastes schlegelii) macrophages as pattern recognition receptors in the antibacterial mechanism of exploration.

As lower vertebrates, fish have both innate and adaptive immune systems, but the role of the adaptive immune system is limited, and the innate immune system plays an important role in the resistance to pathogen infection. C-type lectins (CLRs) are one of the major pattern recognition receptors (PRRs) of the innate immune system. CLRs can combine with pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs) to trigger NF-κB signaling pathway and exert immune efficacy. In this study, Ssclec12b and Ssclec4e of the C-type lectins, were found to be significantly up-regulated in the transcripts of Sebastes schlegelii macrophages stimulated by bacteria. The identification, expression and function of these lectins were studied. In addition, the recombinant proteins of the above two CLRs were obtained by prokaryotic expression. We found that rSsCLEC12B and rSsCLEC4E could bind to a variety of bacteria in a Ca2+-dependent manner, and promoted the agglutination of bacteria and blood cells. rSsCLEC12B and rSsCLEC4E assisted macrophages to recognize PAMPs and activate the NF-κB signaling pathway, thereby promoting the expression of inflammatory factors (TNF-α, IL-1ß, IL-6, IL-8) and regulating the early immune inflammation of macrophages. These results suggested that SsCLEC12B and SsCLEC4E could serve as PRRs in S. schlegelii macrophages to recognize pathogens and participate in the host antimicrobial immune process, and provided a valuable reference for the study of CLRs involved in fish innate immunity.

Genome-wide identification, characterization, molecular evolution and expression profiling analysis of scavenger receptors in black rockfish (Sebastes schlegelii).

The scavenger receptors (SRs) gene family is considered as the membrane-associated pattern recognition receptors that plays important roles in the immune responses of organisms. However, there is currently limited research on the systematic identification of the SRs gene family in teleost and their role in the innate immunity of S. schegelii. In this study, we identified and annotated 15 SRs genes in S. schegelii. Through phylogenetic analysis, analysis of conserved domains, gene structure, and motif composition, we found that SRs gene family within different classes were relatively conserved. Additionally, we used qRT-PCR to analyze the expression patterns of SRs genes in immune-related tissues from healthy and Acinetobacter johnsonii-infected S. schegelii. The results showed that SRs genes exhibited different tissue expression patterns and the expression of SRs genes significantly changed after A. johnsonii infection. These results provided a valuable basis for further understanding of the functions of SRs in the innate immune response of S. schegelii.

Urban-rural disparities in the association of nitrogen dioxide exposure with cardiovascular disease risk in China: effect size and economic burden.

BACKGROUND: Together with rapid urbanization, ambient nitrogen dioxide (NO2) exposure has become a growing health threat. However, little is known about the urban-rural disparities in the health implications of short-term NO2 exposure. This study aimed to compare the association between short-term NO2 exposure and hospitalization for cardiovascular disease (CVD) among urban and rural residents in Shandong Province, China. Then, this study further explored the urban-rural disparities in the economic burden attributed to NO2 and the explanation for the disparities. METHODS: Daily hospitalization data were obtained from an electronic medical records dataset covering a population of 5 million. In total, 303,217 hospital admissions for CVD were analyzed. A three-stage time-series analytic approach was used to estimate the county-level association and the attributed economic burden. RESULTS: For every 10-µg/m3 increase in NO2 concentrations, this study observed a significant percentage increase in hospital admissions on the day of exposure of 1.42% (95% CI 0.92 to 1.92%) for CVD. The effect size was slightly higher in urban areas, while the urban-rural difference was not significant. However, a more pronounced displacement phenomenon was found in rural areas, and the economic burden attributed to NO2 was significantly higher in urban areas. At an annual average NO2 concentration of 10 µg/m3, total hospital days and expenses in urban areas were reduced by 81,801 (44,831 to 118,191) days and 60,121 (33,002 to 86,729) thousand CNY, respectively, almost twice as much as in rural areas. Due to disadvantages in socioeconomic status and medical resources, despite similar air pollution levels in the urban and rural areas of our sample sites, the rural population tended to spend less on hospitalization services. CONCLUSIONS: Short-term exposure to ambient NO2 could lead to considerable health impacts in either urban or rural areas of Shandong Province, China. Moreover, urban-rural differences in socioeconomic status and medical resources contributed to the urban-rural disparities in the economic burden attributed to NO2 exposure. The health implications of NO2 exposure are a social problem in addition to an environmental problem. Thus, this study suggests a coordinated intervention system that targets environmental and social inequality factors simultaneously.

Molecular characterization, expression and immune functional analysis of cystatin 10 in turbot.

BACKGROUND: Cystatin is a protease inhibitor that also regulates genes expression linked to inflammation and plays a role in defense and regulation. METHODS AND RESULTS: Cystatin 10 (Smcys10) was cloned from Scophthalmus maximus and encodes a 145 amino acid polypeptide. The results of qRT-PCR showed that Smcys10 exhibited tissue-specific expression patterns, and its expression was significantly higher in the skin than in other tissues. The expression level of Smcys10 was significantly different in the skin, gill, head kidney, spleen and macrophages after Vibrio anguillarum infection, indicating that Smcys10 may play an important role in resistance to V. anguillarum infection. The recombinant Smcys10 protein showed binding and agglutinating activity in a Ca2+-dependent manner against bacteria. rSmcys10 treatment upregulated the expression of IL-10, TNF-α and TGF-ß in macrophages of turbot and hindered the release of lactate dehydrogenase (LDH) from macrophages after V. anguillarum infection, which confirmed that rSmcys10 reduced the damage to macrophages by V. anguillarum. The NF-κB pathway was suppressed by Smcys10, as demonstrated by dual-luciferase analysis. CONCLUSIONS: These results indicated that Smcys10 is involved in the host antibacterial immune response.

Diagnostic investigation of avian reovirus field variants circulating in broiler chickens in Pennsylvania of United States between 2017 and 2022.

Avian reovirus (ARV) has been continuously affecting the poultry industry in Pennsylvania (PA) in recent years. This report provides our diagnostic investigation on monitoring ARV field variants from broiler chickens in Pennsylvania. Genomic characterization findings of 72 ARV field isolates obtained from broiler cases during the last 6 years indicated that six distinct cluster variant strains (genotype I-VI), which were genetically diverse and distant from the vaccine and vaccine-related field strains, continuously circulated in PA poultry. Most of the variants clustered within genotype V (24/72, 33.3%), followed by genotype II (16/72, 22.2%), genotype IV (13/72, 18.1%), genotype III (13/72, 18.1%), genotype VI (05/72, 6.94%), and genotype I (1/72, 1.38%). The amino acid identity between 72 field variants and the vaccine strains (1133, 1733, 2408, 2177) varied from 45.3% to 99.7%, while the difference in amino acid counts ranged from 1-164. Among the field variants, the amino acid identity and count difference ranged from 43.3% to 100% and 0 to 170, respectively. Variants within genotype V had maximum amino acid identity (94.7-100%), whereas none of the variants within genotypes II and VI were alike. These findings indicate the continuing occurrence of multiple ARV genotypes in the environment.

Nonbiodegradable microplastic types determine the diversity and structure of soil microbial communities: A meta-analysis.

As an emerging contaminant, microplastics (MPs) have received considerable attention for their potential threat to the soil environment. However, the response of soil bacterial and fungal communities to MPs exposure remains unclear. In this study, we conducted a global meta-analysis of 95 publications and 2317 observations to assess the effects of nonbiodegradable MP properties and exposure conditions on soil microbial biomass, alpha and beta diversity, and community structure. Our results indicate that MPs increased (p < 0.05) soil active microbial biomass by 42%, with the effect varying with MPs type, exposure concentration, exposure time and soil pH. MPs concentration was identified as the most important factor controlling the response of soil microbial biomass to MPs. MPs addition decreased (p < 0.05) the soil bacterial Shannon and Chao1 indices by 2% and 3%, respectively, but had limited effects (p > 0.05) on soil fungal Shannon and Chao1 indices. The type of MPs and exposure time determined the effects of MPs on bacterial Shannon and Chao1 indices, while the type of MPs and soil pH controlled the response ratios of fungal Shannon and Chao1 indices to MPs. Specifically, soil organic carbon (SOC) was the major factor regulating the response ratio of bacterial alpha diversity index to MPs. The presence of MPs did not affect soil bacterial community structure and beta diversity. Our results highlight that MPs reduced bacterial diversity and richness but increased the soil active microbial biomass, suggesting that MPs could disrupt biogeochemical cycles by promoting the growth of specific microorganisms.

Transforming growth factor-ß (TGF-ß): A master signal pathway in teleost sex determination.

Sex determination and differentiation in fish has always been a hot topic in genetic breeding of aquatic animals. With the advances in next-generation sequencing (NGS) in recent years, sex chromosomes and sex determining genes can be efficiently identified in teleosts. To date, master sex determination genes have been elucidated in 114 species, of which 72 species have sex determination genes belonging to TGF-ß superfamily. TGF-ß is the only signaling pathway that the largest proportion of components, which including ligands (amhy, gsdfy, gdf6), receptors (amhr, bmpr), and regulator (id2bby), have opportunity recognized as a sex determination gene. In this review, we focus on the recent studies about teleost sex-determination genes within TGF-ß superfamily and propose several hypotheses on how these genes regulate sex determination process. Differing from other reviews, our review specifically devotes significant attention to all members of the TGF-ß signal pathway, not solely the sex determination genes within the TGF-ß superfamily. However, the functions of the paralogous genes of TGF superfamily are still needed ongoing research. Further studies are required to more accurately interpret the molecular mechanism of TGF-ß superfamily sex determination genes.