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In this study, red mud modified by manganese dioxide(MRM) was utilized as an adsorbent to effectively remove Cd 2+ from aqueous solution. The characteristics were analysed by SEM–EDS, XRD, BET, FTIR and XPS. Different factors that affected the Cd 2+ removal on MRM, such as dosage, initial pH, initial Cd 2+ concentration, were investigated using batch adsorption experiments. Simultaneously, the adsorption kinetics, adsorption isotherms and adsorption thermodynamics of Cd 2+ were also investigated using adsorption experiments data. The characterization results showed that MRM had a rougher, larger specific surface area and pore volume (38.91 m 2 g −1 , 0.02 cm 3 g −1 ) than RM (10.22 m 2 g −1 , 0.73 cm 3 g −1 ). The adsorption experiments found that the equilibrium adsorption capacity of MRM for Cd 2+ was significantly increased to 46.36 mg g −1 , which was almost three times that of RM. According to the fitting results, the pseudo-second-order kinetic model described the adsorption process better than the pseudo-first-order kinetic model. The Langmuir model fitted the adsorption isotherms well, indicating that the adsorption process was unimolecular layer adsorption and the maximum capacity was 103.59 mg g −1 . The thermodynamic parameters indicated that the adsorption process was heat-trapping and spontaneous. Finally, combined XPS and FTIR studies, it was speculated that the adsorption mechanisms should be electrostatic attachment, specific adsorption (i.e., Cd–O or hydroxyl binding) and ion exchange. Therefore, manganese dioxide modified red mud can be an effective and economical alternative to the removal of Cd 2+ in the wastewater treatment process.

Background Parkinson’s disease (PD) is characterized by dopaminergic neuronal loss in the substantia nigra pars compacta and intracellular inclusions called Lewy bodies (LB). During the course of disease, misfolded α-synuclein, the major constituent of LB, spreads to different regions of the brain in a prion-like fashion, giving rise to successive non-motor and motor symptoms. Etiology is likely multifactorial, and involves interplay among aging, genetic susceptibility and environmental factors. Main body The prevalence of PD rises exponentially with age, and aging is associated with impairment of cellular pathways which increases susceptibility of dopaminergic neurons to cell death. However, the majority of those over the age of 80 do not have PD, thus other factors in addition to aging are needed to cause disease. Discovery of neurotoxins which can result in parkinsonism led to efforts in identifying environmental factors which may influence PD risk. Nevertheless, the causality of most environmental factors is not conclusively established, and alternative explanations such as reverse causality and recall bias cannot be excluded. The lack of geographic clusters and conjugal cases also go against environmental toxins as a major cause of PD. Rare mutations as well as common variants in genes such as SNCA, LRRK2 and GBA are associated with risk of PD, but Mendelian causes collectively only account for 5% of PD and common polymorphisms are associated with small increase in PD risk. Heritability of PD has been estimated to be around 30%. Thus, aging, genetics and environmental factors each alone is rarely sufficient to cause PD for most patients. Conclusion PD is a multifactorial disorder involving interplay of aging, genetics and environmental factors. This has implications on the development of appropriate animal models of PD which take all these factors into account. Common converging pathways likely include mitochondrial dysfunction, impaired autophagy, oxidative stress and neuroinflammation, which are associated with the accumulation and spread of misfolded α-synuclein and neurodegeneration. Understanding the mechanisms involved in the initiation and progression of PD may lead to potential therapeutic targets to prevent PD or modify its course.

Plants possess cell surface-localized immune receptors that detect microbe-associated molecular patterns (MAMPs) and initiate defenses that provide effective resistance against microbial pathogens. Many MAMP-induced signaling pathways and cellular responses are known, yet how pattern-triggered immunity (PTI) limits pathogen growth in plants is poorly understood. Through a combined metabolomics and genetics approach, we discovered that plant-exuded proline is a virulence-inducing signal and nutrient for the bacterial pathogen Pseudomonas syringae , and that MAMP-induced depletion of proline from the extracellular spaces of Arabidopsis leaves directly contributes to PTI against P. syringae . We further show that MAMP-induced depletion of extracellular proline requires the amino acid transporter L ysine H istidine T ransporter 1 (LHT1). This study demonstrates that depletion of a single extracellular metabolite is an effective component of plant induced immunity. Given the important role for amino acids as nutrients for microbial growth, their depletion at sites of infection may be a broadly effective means for defense against many pathogens. Plant pathogenic bacteria use host metabolites as virulence cues and nutrients. Here, Rogan et al. show that proline is depleted from the extracellular spaces of immune-elicited Arabidopsis leaves and that this depletion limits the growth of Pseudomonas syringae .

Pathogenic bacteria frequently acquire virulence traits via horizontal gene transfer, yet additional evolutionary innovations may be necessary to integrate newly acquired genes into existing regulatory pathways. The plant bacterial pathogen Pseudomonas syringae relies on a horizontally acquired type III secretion system (T3SS) to cause disease. T3SS-encoding genes are induced by plant-derived metabolites, yet how this regulation occurs, and how it evolved, is poorly understood. Here we report that the two-component system AauS-AauR and substrate-binding protein AatJ, proteins encoded by an acidic amino acid-transport (aat) and -utilization (aau) locus in P. syringae, directly regulate T3SS-encoding genes in response to host aspartate and glutamate signals. Mutants of P. syringae strain DC3000 lacking aauS, aauR or aatJ expressed lower levels of T3SS genes in response to aspartate and glutamate, and had decreased T3SS deployment and virulence during infection of Arabidopsis. We identified an AauR-binding motif (Rbm) upstream of genes encoding T3SS regulators HrpR and HrpS, and demonstrated that this Rbm is required for maximal T3SS deployment and virulence of DC3000. The Rbm upstream of hrpRS is conserved in all P. syringae strains with a canonical T3SS, suggesting AauR regulation of hrpRS is ancient. Consistent with a model of conserved function, an aauR deletion mutant of P. syringae strain B728a, a bean pathogen, had decreased T3SS expression and growth in host plants. Together, our data suggest that, upon acquisition of T3SS-encoding genes, a strain ancestral to P. syringae co-opted an existing AatJ-AauS-AauR pathway to regulate T3SS deployment in response to specific host metabolite signals.

The type VI secretion system (T6SS) is a widespread protein secretion system found in many Gram-negative bacteria. T6SSs are highly regulated by various regulatory systems at multiple levels, including post-translational regulation via threonine (Thr) phosphorylation. The Ser/Thr protein kinase PpkA is responsible for this Thr phosphorylation regulation, and the forkhead-associated (FHA) domain-containing Fha-family protein is the sole T6SS phosphorylation substrate identified to date. Here we discovered that TssL, the T6SS inner-membrane core component, is phosphorylated and the phosphorylated TssL (p-TssL) activates type VI subassembly and secretion in a plant pathogenic bacterium, Agrobacterium tumefaciens. Combining genetic and biochemical approaches, we demonstrate that TssL is phosphorylated at Thr 14 in a PpkA-dependent manner. Further analysis revealed that the PpkA kinase activity is responsible for the Thr 14 phosphorylation, which is critical for the secretion of the T6SS hallmark protein Hcp and the putative toxin effector Atu4347. TssL phosphorylation is not required for the formation of the TssM-TssL inner-membrane complex but is critical for TssM conformational change and binding to Hcp and Atu4347. Importantly, Fha specifically interacts with phosphothreonine of TssL via its pThr-binding motif in vivo and in vitro and this interaction is crucial for TssL interaction with Hcp and Atu4347 and activation of type VI secretion. In contrast, pThr-binding ability of Fha is dispensable for TssM structural transition. In conclusion, we discover a novel Thr phosphorylation event, in which PpkA phosphorylates TssL to activate type VI secretion via its direct binding to Fha in A. tumefaciens. A model depicting an ordered TssL phosphorylation-induced T6SS assembly pathway is proposed.

This study provides a fresh understanding of the historical development shaping comparative studies between Christianity and Mohism during the late Qing and Republican China periods. It traces the foundation of these studies to both the idea that ‘Western knowledge originated from Mohism’ and to the Mohism studies by the Qian-Jia School 乾嘉學派 during the Qing Dynasty. This study spotlights the groundbreaking proposition by Zou Boqi 鄒伯奇 in 1844, who first suggested that Western knowledge, including Christianity, originated from Mohism, a widely accepted view among Chinese literati. The article then explores the paradigm shift initiated by Liang Qichao 梁啓超, influenced by Sun Yirang 孫詒讓 and his Mozi Jiangu 墨子閒詁 (The Works of Mozi with Commentaries), which broadened the comparative perspective. The significant influence of the Qian-Jia School’s Mohism studies on both Chinese and non-Chinese scholars is analyzed, along with the diverse approaches and contributions of key figures like Joesph Edkins, James Legge, Ernst Faber, Alexandra David-Néel, Daisetz Teitaro Suzuki, Huang Zhiji 黃治基, Wang Zhixin 王治心, Zhang Chunyi 張純一, Mei Yi-Pao 梅貽寶, and Wu Leichuan 吳雷川. The article underscores these scholarly groups’ dynamic interplay and varied objectives, shaping a vibrant and contentious academic landscape.

Tail-anchored (TA) proteins are involved in cellular processes including trafficking, degradation, and apoptosis. They contain a C-terminal membrane anchor and are posttranslationally delivered to the endoplasmic reticulum (ER) membrane by the Get3 adenosine triphosphatase interacting with the hetero-oligomeric Get1/2 receptor. We have determined crystal structures of Get3 in complex with the cytosolic domains of Get1 and Get2 in different functional states at 3.0, 3.2, and 4.6 angstrom resolution. The structural data, together with biochemical experiments, show that Get1 and Get2 use adjacent, partially overlapping binding sites and that both can bind simultaneously to Get3. Docking to the Get1/2 complex allows for conformational changes in Get3 that are required for TA protein insertion. These data suggest a molecular mechanism for nucleotide-regulated delivery of TA proteins.

Mutations in leucine-rich repeat kinase 2 ( LRRK2 ) and glucocerebrosidase ( GBA ) represent two most common genetic causes of Parkinson’s disease (PD). Both genes are important in the autophagic-lysosomal pathway (ALP), defects of which are associated with α-synuclein (α-syn) accumulation. LRRK2 regulates macroautophagy via activation of the mitogen activated protein kinase/extracellular signal regulated protein kinase (MAPK/ERK) kinase (MEK) and the calcium-dependent adenosine monophosphate (AMP)-activated protein kinase (AMPK) pathways. Phosphorylation of Rab GTPases by LRRK2 regulates lysosomal homeostasis and endosomal trafficking. Mutant LRRK2 impairs chaperone-mediated autophagy, resulting in α-syn binding and oligomerization on lysosomal membranes. Mutations in GBA reduce glucocerebrosidase (GCase) activity, leading to glucosylceramide accumulation, α-syn aggregation and broad autophagic abnormalities. LRRK2 and GBA influence each other: GCase activity is reduced in LRRK2 mutant cells, and LRRK2 kinase inhibition can alter GCase activity in GBA mutant cells. Clinically, LRRK2 G2019S mutation seems to modify the effects of GBA mutation, resulting in milder symptoms than those resulting from GBA mutation alone. However, dual mutation carriers have an increased risk of PD and earlier age of onset compared with single mutation carriers, suggesting an additive deleterious effect on the initiation of PD pathogenic processes. Crosstalk between LRRK2 and GBA in PD exists, but its exact mechanism is unclear. Drugs that inhibit LRRK2 kinase or activate GCase are showing efficacy in pre-clinical models. Since LRRK2 kinase and GCase activities are also altered in idiopathic PD (iPD), it remains to be seen if these drugs will be useful in disease modification of iPD.

The identification and genomic editing of defense‐related genes to confer resistance to pathogens is an effective and promising strategy for use in crop breeding. However, resistance is often associated with growth inhibition, a phenomenon referred to as the “trade‐off” effect, making enhancing resistance without sacrificing yield challenging. In this study, a novel strategy is presented to enhance broad‐spectrum resistance in crops without yield loss by editing susceptibility lncRNAs. RESIS, a pathogen‐induced lncRNA that acquired its function in the pathogen response during domestication, is identified. Upon pathogen invasion, RESIS is activated by effector‐binding elements on its promoter and subsequently binds to NAA15 and NAA10, two core components of the NatA complex. RESIS enables NAA10 to interact with NAA15 through a sequence that evolves in cultivated rice, enhancing the activity of the NatA complex in the N‐terminal acetylation of proteins. RESIS knockout suppresses this process and increases translation during pathogen invasion, conferring resistance to both fungal and bacterial diseases without the growth inhibition typically associated with the direct knockout of the NatA complex. These findings highlight the potential of susceptibility lncRNAs as promising target loci for improving crop broad‐spectrum disease resistance without detrimental effects on growth, offering significant prospects for practical applications. Editing susceptibility lncRNAs offers a strategy to enhance disease resistance without yield loss. RESIS, a domestication‐acquired, pathogen‐induced lncRNA, promotes protein N‐terminal acetylation through its interaction with NatA complex. Knockout of RESIS increases translation and confers broad‐spectrum resistance to both fungal and bacterial pathogens without causing growth inhibition, highlighting its potential as a valuable target for crop improvement.

Polymorphisms in TMEM106B, a gene on chromosome 7p21.3 involved in lysosomal trafficking, correlates to worse neuropathological, and clinical outcomes in frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS) with TDP‐43 inclusions. In a small cohort of C9orf72 expansion carriers, we previously found an atypical, neuroglial tauopathy in cases harboring a TMEM106B rs1990622 A/A genotype. To test whether TMEM106B genotype affects the risk of developing atypical tauopathy under a recessive genotype model (presence versus absence of two major alleles: A/A vs. A/G and G/G). We characterized the atypical tauopathy neuropathologically and determined its frequency by TMEM106B rs1990622 genotypes in 90 postmortem cases with a primary diagnosis of FTLD/ALS‐TDP [mean age at death 65.5 years (±8.1), 40% female]. We investigated the effect of this new atypical tauopathy on demographics and clinical and neuropsychological metrics. We also genotyped TMEM106B in an independent series with phenotypically similar cases. Sixteen cases (16/90, 17.7 %) showed the temporal‐predominant neuro‐astroglial tauopathy, and 93.7% of them carried an A/A genotype (vs. ~35% in a population cohort). The odds ratio of FTLD/ALS‐TDP individuals with the A/A genotype showing neuro‐astroglial tauopathy was 13.9. Individuals with this tauopathy were older at onset (p = 0.01). The validation cohort had a similarly high proportion of rs1990622 A/A genotype. TDP‐43 and tau changes co‐occur in a subset of neurons. Our data add to the growing body of evidence that TMEM106B polymorphisms may modulate neurodegeneration. A distinctive medial temporal predominant, 4‐repeat, neuro‐astroglial tauopathy strongly correlates to TMEM106B A/A genotype in FTLD/ALS‐TDP cases. noFTLD‐TDP cases with a TMEM106b A/A genotype have a much‐increased odds to show a distinct temporal‐predominant neuro‐astroglial tauopahty.