氮沉降背景下土壤微生物对入侵植物乌桕叶绿素荧光特征的影响

植物入侵会造成入侵地生态系统功能和稳定性的破坏。与原产地种源相比,入侵种源植物在生理学特性方面有所不同,使其在资源利用和抵抗环境胁迫具有较强的竞争优势。叶绿素荧光特性与植物光合作用效率密切相关,对植物生长具有重要作用。氮沉降加剧是全球变化的一个重要因子,土壤微生物对植物吸收利用土壤养分至关重要。通过施用细菌抑制剂（链霉素）和真菌抑制剂（扑海因）选择性抑制的土壤微生物活性,开展乌桕盆栽实验,在模拟氮沉降背景下,研究不同微生物群落如何影响入侵乌桕叶绿素荧光特性,有助于理解入侵植物的进化特征和入侵机制,为有效防控入侵植物并降低其对生态系统危害提供理论依据。以原产地地和入侵地两个种源乌桕（Triadica sebifera）为研究对象,在氮沉降条件下,通过调控土壤细菌和真菌,探讨两个种源乌桕叶绿素荧光参数差异。结果显示：氮沉降显著增加乌桕相对叶绿素含量（SPAD）、光系统II的最大量子产率（F_v/F_m）、非光化学猝灭（NPQ）和半饱和光强（I_k）。入侵种源乌桕比原产地具有较低SPAD。氮沉降与细菌抑制剂共同作用显著增强了F_v/F_m、NPQ和I_k,显著减弱了光能利用率（α）和SPAD。细菌抑制剂减缓了本地种源乌桕α,真菌抑制剂促进本地种源乌桕I_k,抑制入侵种源乌桕I_k,细菌和真菌抑制剂可显著降低原产地乌桕α。氮沉降与生物抑制剂可显著作用于乌桕叶片SPAD。氮沉降、土壤微生物和不同乌桕种源可共同作用于光系统Ⅱ实际光合量子产率Y（Ⅱ）,α和潜在最大相对电子传递速率（ETR_max）。因此,氮沉降与生物抑制剂对乌桕叶绿素荧光特性具有协同作用,入侵种源乌桕对土壤微生物控制的响应不明显,在微生物控制条件下依然具有较强的适应能力,因而具有较强的入侵能力。     

GDF11 prevents the formation of thoracic aortic dissection in mice: Promotion of contractile transition of aortic SMCs

Thoracic aortic dissection (TAD) is an aortic disease associated with dysregulated extracellular matrix composition and de-differentiation of vascular smooth muscle cells (SMCs). Growth Differentiation Factor 11 (GDF11) is a member of transforming growth factor β (TGF-β) superfamily associated with cardiovascular diseases. The present study attempted to investigate the expression of GDF11 in TAD and its effects on aortic SMC phenotype transition. GDF11 level was found lower in the ascending thoracic aortas of TAD patients than healthy aortas. The mouse model of TAD was established by β-aminopropionitrile monofumarate (BAPN) combined with angiotensin II (Ang II). The expression of GDF11 was also decreased in thoracic aortic tissues accompanied with increased inflammation, arteriectasis and elastin degradation in TAD mice. Administration of GDF11 mitigated these aortic lesions and improved the survival rate of mice. Exogenous GDF11 and adeno-associated virus type 2 (AAV-2)-mediated GDF11 overexpression increased the expression of contractile proteins including ACTA2, SM22α and myosin heavy chain 11 (MYH11) and decreased synthetic markers including osteopontin and fibronectin 1 (FN1), indicating that GDF11 might inhibit SMC phenotype transition and maintain its contractile state. Moreover, GDF11 inhibited the production of matrix metalloproteinase (MMP)-2, 3, 9 in aortic SMCs. The canonical TGF-β (Smad2/3) signalling was enhanced by GDF11, while its inhibition suppressed the inhibitory effects of GDF11 on SMC de-differentiation and MMP production in vitro. Therefore, we demonstrate that GDF11 may contribute to TAD alleviation via inhibiting inflammation and MMP activity, and promoting the transition of aortic SMCs towards a contractile phenotype, which provides a therapeutic target for TAD.     

Mitochondrial phosphatase PGAM5 regulates Keap1-mediated Bcl-xL degradation and controls cardiomyocyte apoptosis driven by myocardial ischemia/reperfusion injury

Phosphoglycerate mutase 5 (PGAM5) is a mitochondrial membrane protein that plays crucial roles in necroptosis and apoptosis. Though PGAM5 is known to be required for inducing intrinsic apoptosis through interacting with BCL2 associated X protein (Bax) and dynamin-related protein 1 (Drp1), the expression and role of PGAM5 in cardiomyocyte apoptosis driven by myocardial ischemia/reperfusion injury(MIRI) has not been studied. The present study shows that PGAM5 expression decreased after MIRI in vivo, positively correlated with Bcl-xL expression, negatively correlated with Kelch-ECH associating protein 1 (Keap1) expression. Furthermore, PGAM5 expression also decreased in cardiomyocytes after hypoxia/reoxygenation (H/R) treatment in vitro. PGAM5 silence promoted cardiomyocyte apoptosis and inhibited Bcl-xL expression, but with no effect on Keap1 expression. Accordingly, Keap1 overexpression further inhibited Bcl-xL and PGAM5 expression. Additionally, PGAM5-Bcl-xL-Keap1 interaction was identified, suggesting that PGAM5 might participate in the degradation of Bcl-xL mediated by Keap1. In summary, PGAM5 controls cardiomyocyte apoptosis induced by MIRI through regulating Keap1-mediated Bcl-xL degradation, which may supply a novel molecular target for acute myocardial infarction (AMI) therapy.

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细菌冰核提高印度谷螟过冷却点的研究

印度谷螟(Plodia interpunctella)是一种不耐结冰的昆虫,在冬季它通过降低过冷却 点以避免结冰。现已查明,冰核活性细菌能显著提高植物的过冷却点,导致许多作物在较高 的温度下发生霜冻害。本文也证明细菌冰核能显著提高印度谷螟虫的过冷却点。对照的平均过冷却点是-17.6℃;分别用0.1g和1g细菌冰核与1kg面粉混合后进行处理,平均过冷却点分别比对照提高了12.8℃和13.6℃。研究结果支持这样的观点：细菌冰核有可能成为一种在冬季使用的、杀灭不耐结冰害虫的生物制剂。     

细菌冰核提高印度谷螟过冷却点的研究

印度谷螟（Ｐｌｏｄｉａｉｎｔｅｒｐｕｎｃｔｅｌｌａ）是一种不耐结冰的昆虫,在冬季它通过降低过冷却点以避免结冰。现已查明,冰核活性细菌能显著提高植物的过冷却点,导致许多作物在较高的温度下发生霜冻害。本文也评明细菌冰核能显著提高印度谷螟幼虫的过冷却点。对照的平均过冷却点是－１７．６℃;分别用０．１ｇ和１ｇ细菌冰核与１ｋｇ面粉混合后进行处理,平均过冷却点分别比对照提高了１２．８℃和１３．６℃。研究结果支持这样的观点：细菌冰核有可能成为一种在冬季使用的、杀灭不耐结冰害虫的生物制剂。     

Vacuolar (H)-ATPases in Caenorhabditis elegans: What can we learn about giant H pumps from tiny worms?

Vacuolar (H⁺)-ATPases, also called V-ATPases, are ATP-driven proton pumps that are highly phylogenetically conserved. Early biochemical and cell biological studies have revealed many details of the molecular mechanism of proton pumping and of the structure of the multi-subunit membrane complex, including the stoichiometry of subunit composition. In addition, yeast and mouse genetics have broadened our understanding of the physiological consequences of defective vacuolar acidification and its related disease etiologies. Recently, phenotypic investigation of V-ATPase mutants in Caenorhabditis elegans has revealed unexpected new roles of V-ATPases in both cellular function and early development. In this review, we discuss the functions of the V-ATPases discovered in C. elegans.     

UV Raman monitoring of histidine protonation and H-(2)H exchange in plastocyanin

UV resonance Raman bands of Cu-bound and protonated histidine residues have been detected in (2)H(2)O solutions of poplar plastocyanin. For the Cu(II) protein, slow NH-(2)H exchange of the His37 ligand was monitored via the growth of bands at 1389 and 1344 cm(-1) when Pcy was exchanged into (2)H(2)O, or via their diminution when the protein was exchanged back into H(2)O; the rate constant is 7 x 10(-4)/s at pH (p(2)H) 7.4 at room temperature. The slow exchange is attributed to imidazole H-bonding to a backbone carbonyl. Nearby bands at 1397 and 1354 cm(-1), appear and disappear within the mixing time, and are assigned to the solvent-exposed His87 ligand. The approximately 10 cm(-1) differences between His37 and His87 are attributed to the effect of H-bonding on the imidazole ring modes. The UVRR spectra of the Cu(I) protein in (2)H(2)O reveal a 1408 cm(-1) band, characteristic of NH-(2)H-exchanged histidinium, which grows in as the p(2)H is lowered. Its intensity follows a titration curve with pK(a)=4.6. This protonation is assigned to the His87 residue, whose bond to the Cu(I) is known from crystallography to be broken at low pH. As the 1408 cm(-1) band grows, a band at 1345 cm(-1) diminishes, while another, at 1337 cm(-1) stays constant. These are assigned to modes of bound His87 and His37, respectively, shifted down 7-9 cm(-1) from their Cu(II) positions.