Depth‐dependent soil organic carbon dynamics of croplands across the Chengdu Plain of China from the 1980s to the 2010s

Agricultural soils have tremendous potential to sequester soil organic carbon (SOC) and mitigate global climate change. However, agricultural land use has a profound impact on SOC dynamics, and few studies have explored how agricultural land use combined with soil conditions affect SOC changes throughout the soil profile. Based on a paired soil resampling campaign in the 1980s and 2010s, this study investigated the SOC changes of the soil profile caused by agricultural land use and the correlations with parent material and topography across the Chengdu Plain of China. The results showed that the SOC content increased by 3.78 g C/kg in the topsoil (0–20 cm), but decreased in the 20–40 cm and 40–60 cm soil layers by 0.90 and 1.26 g C/kg respectively. SOC increases in topsoil were observed for all types of agricultural land. Afforestation on former agricultural land also caused SOC decreases in the 20–60 cm soil layers, while SOC decreases only occurred in the 40–60 cm soil layer for agricultural land using a traditional crop rotation (i.e. traditional rice–wheat/rapeseed rotation) and with rice–vegetable rotations converted from the traditional rotations. For each agricultural land use, SOC decreases in deep soils only occurred in high relief areas and in soils formed from Q4 (Quaternary Holocene) grey‐brown alluvium and Q4 grey alluvium that had a relatively low soil bulk density and clay content. The results indicated that SOC change caused by agricultural land use was depth dependent and that the effects of agricultural land use on soil profile SOC dynamics varied with soil characteristics and topography. Subsoil SOC decreases were more likely to occur in high relief areas and in soils with low soil bulk density and low clay content.     

Agrobacterium tumefaciens ferritins play an important role in full virulence through regulating iron homeostasis and oxidative stress survival

Ferritins are a large family of iron storage proteins, which are used by bacteria and other organisms to avoid iron toxicity and as a safe iron source in the cytosol. Agrobacterium tumefaciens, a phytopathogen, has two ferritin-encoding genes: atu2771 and atu2477. Atu2771 is annotated as a Bfr-encoding gene (Bacterioferritin, Bfr) and atu2477 as a Dps-encoding gene (D NA binding p rotein from s tarved cells, Dps). Three deletion mutants (Δbfr, Δdps, and bfr-dps double-deletion mutant ΔbdF) of these two ferritin-encoding genes were constructed to investigate the effects of ferritin deficiency on the iron homeostasis, oxidative stress resistance, and pathogenicity of A. tumefaciens. Deficiency of two ferritins affects the growth of A. tumefaciens under iron starvation and excess. When supplied with moderate iron, the growth of A. tumefaciens is not affected by the deficiency of ferritin. Deficiency of ferritin significantly reduces iron accumulation in the cells of A. tumefaciens, but the effect of Bfr deficiency on iron accumulation is severer than Dps deficiency and the double mutant ΔbdF has the least intracellular iron content. All three ferritin-deficient mutants showed a decreased tolerance to 3 mM H₂O₂ in comparison with the wild type. The tumour induced by each of three ferritin-deficient mutants is less than that of the wild type. Complementation reversed the effects of ferritin deficiency on the growth, iron homeostasis, oxidative stress resistance, and tumorigenicity of A. tumefaciens. Therefore, ferritin plays an important role in the pathogenesis of A. tumefaciens through regulating iron homeostasis and oxidative stress survival.     

The cis-expression of the coat protein of turnip mosaic virus is essential for viral intercellular movement in plants

To establish infection, plant viruses are evolutionarily empowered with the ability to spread intercellularly. Potyviruses represent the largest group of known plant-infecting RNA viruses, including many agriculturally important viruses. To better understand intercellular movement of potyviruses, we used turnip mosaic virus (TuMV) as a model and constructed a double-fluorescent (green and mCherry) protein-tagged TuMV infectious clone, which allows distinct observation of primary and secondary infected cells. We conducted a series of deletion and mutation analyses to characterize the role of TuMV coat protein (CP) in viral intercellular movement. TuMV CP has 288 amino acids and is composed of three domains: the N-terminus (amino acids 1–97), the core (amino acids 98–245), and the C-terminus (amino acids 246–288). We found that deletion of CP or its segments amino acids 51–199, amino acids 200–283, or amino acids 265–274 abolished the ability of TuMV to spread intercellularly but did not affect virus replication. Interestingly, deletion of amino acids 6–50 in the N-terminus domain resulted in the formation of aberrant virions but did not significantly compromise TuMV cell-to-cell and systemic movement. We identified the charged residues R178 and D222 within the core domain that are essential for virion formation and TuMV local and systemic transport in plants. Moreover, we found that trans-expression of the wild-type CP either by TuMV or through genetic transformation-based stable expression could not rescue the movement defect of CP mutants. Taken together these results suggest that TuMV CP is not essential for viral genome replication but is indispensable for viral intercellular transport where only the cis-expressed CP is functional.     

Functional analyses of small secreted cysteine-rich proteins identified candidate effectors in Verticillium dahliae

Secreted small cysteine-rich proteins (SCPs) play a critical role in modulating host immunity in plant–pathogen interactions. Bioinformatic analyses showed that the fungal pathogen Verticillium dahliae encodes more than 100 VdSCPs, but their roles in host–pathogen interactions have not been fully characterized. Transient expression of 123 VdSCP-encoding genes in Nicotiana benthamiana identified three candidate genes involved in host–pathogen interactions. The expression of these three proteins, VdSCP27, VdSCP113, and VdSCP126, in N. benthamiana resulted in cell death accompanied by a reactive oxygen species burst, callose deposition, and induction of defence genes. The three VdSCPs mainly localized to the periphery of the cell. BAK1 and SOBIR1 (associated with receptor-like protein) were required for the immunity triggered by these three VdSCPs in N. benthamiana. Site-directed mutagenesis showed that cysteine residues that form disulphide bonds are essential for the functioning of VdSCP126, but not VdSCP27 and VdSCP113. VdSCP27, VdSCP113, and VdSCP126 individually are not essential for V. dahliae infection of N. benthamiana and Gossypium hirsutum, although there was a significant reduction of virulence on N. benthamiana and G. hirsutum when inoculated with the VdSCP27/VdSCP126 double deletion strain. These results illustrate that the SCPs play a critical role in the V. dahliae–plant interaction via an intrinsic virulence function and suppress immunity following infection.     

Tle1 attenuates hepatic ischemia/reperfusion injury by suppressing NOD2/NF-κB signaling

ABSTRACT

Liver damage induced by ischemia/reperfusion (I/R) remains a primary issue in multiple hepatic surgeries. Innate immune-mediated inflammatory responses during the reperfusion stage aggravate the injury. Nevertheless, the detailed mechanism of hepatic I/R has not been fully clarified yet. Our research focuses on the role of Transducin-like enhancer of split-1 (Tle1) in the liver I/R injury and the relation between Tle1 and Nucleotide-binding oligomerization domain 2 (NOD2). To answer these questions, we constructed mouse models of I/R and cell models of hypoxia/reoxygenation (H/R). We found decreased Tle1 accompanied by increased NOD2 during reperfusion. Mice pro-injected with Tle1-siRNA emerged aggravated liver dysfunction. Repression of Tle1 had a significant impact on NOD2 and downstream NF-κB signaling in vitro. However, alteration of NOD2 failed to affect the expression of Tle1. To conclude, our study demonstrates that Tle1 shelters the liver from I/R injury through suppression of NOD2-dependent NF-κB activation and subsequent inflammatory responses.     

两种价态铬(Ⅲ,Ⅵ)对真核酵母细胞谷胱甘肽水平影响

工业的迅猛发展使得重金属污染加剧,得到了人们的广泛关注。铬(Cr)在化工业中的广泛应用,使其成为一种主要的环境污染重金属离子。酿酒酵母是研究金属毒性最常用的生物之一。本文比较了三种铬盐(三氯化铬、三氧化铬、重铬酸钾)对酿酒酵母生长的影响,半抑制浓度的两种价态铬(Cr^3+,Cr^6+)处理酵母细胞,Cr^6+引起细胞的致死率更高。已有研究表明谷胱甘肽是胞内重要的还原剂,常用于细胞的重金属解毒,因此探究了两种价态的铬对酵母胞内谷胱甘肽水平的影响。结果显示重铬酸钾和三氧化铬浓度的升高都会引起胞内含量显著降低,而三氯化铬基本不变,过表达GSH1基因有利于提高酵母细胞对Cr^6+的抗性,但对Cr^3+没有明显效果,这说明两种价态铬在胞内生化作用方式不同,细胞应对的解毒机制也不一样。该研究对工业含铬废弃物处理和微生物治理环境污染提供了理论依据。