Traits mediate drought effects on wood carbon fluxes

CO₂ fluxes from wood decomposition represent an important source of carbon from forest ecosystems to the atmosphere, which are determined by both wood traits and climate influencing the metabolic rates of decomposers. Previous studies have quantified the effects of moisture and temperature on wood decomposition, but these effects were not separated from the potential influence of wood traits. Indeed, it is not well understood how traits and climate interact to influence wood CO₂ fluxes. Here, we examined the responses of CO₂ fluxes from dead wood with different traits (angiosperm and gymnosperm) to 0%, 35%, and 70% rainfall reduction across seasonal temperature gradients. Our results showed that drought significantly decreased wood CO₂ fluxes, but its effects varied with both taxonomical group and drought intensity. Drought‐induced reduction in wood CO₂ fluxes was larger in angiosperms than gymnosperms for the 35% rainfall reduction treatment, but there was no significant difference between these groups for the 70% reduction treatment. This is because wood nitrogen density and carbon quality were significantly higher in angiosperms than gymnosperms, yielding a higher moisture sensitivity of wood decomposition. These findings were demonstrated by a significant positive interaction effect between wood nitrogen and moisture on CO₂ fluxes in a structural equation model. Additionally, we ascertained that a constant temperature sensitivity of CO₂ fluxes was independent of wood traits and consistent with previous estimates for extracellular enzyme kinetics. Our results highlight the key role of wood traits in regulating drought responses of wood carbon fluxes. Given that both climate and forest management might extensively modify taxonomic compositions in the future, it is critical for carbon cycle models to account for such interactions between wood traits and climate in driving dynamics of wood decomposition.     

The Water-Soluble Pool in Biochar Dominates Maize Plant Growth Promotion Under Biochar Amendment

Although amending biochar into agricultural soils has been regarded as an effective measure to improve crop productivity, it remains unclear why biochar increases crop yield. The objective of this study was to compare the relative contribution of different biochar components in crop growth promotion. Three biochar components were separated: (i) water-soluble biochar extract (BE), (ii) mineral nutrients from biochar ash (BA), and (iii) washed biochar residue (WB). Two soils (Anthrosol and Primosol) with distinctly different organic carbon content, soil texture and land use were amended with the three biochar components and their effects on maize (Zea mays L.) growth were tested in a pot experiment. We hypothesized that (1) plant grown in the Anthrosol benefitted more from the water-soluble compounds of biochar than from its mineral nutrients or washed residue, since the soil is already fertile and has a good structure; (2) plant grown in the Primosol benefitted more from the mineral nutrients of biochar and its washed residual, since the soil is nutrient-poor and has a poor structure. The addition of biochar and its three components increased maize aboveground biomass for both soils. In the Anthrosol, BE, BA, and WB increased the aboveground biomass by 41.6%, 32.7%, and 27.1%; in the Primosol, they increased the aboveground biomass by 41.3%, 24.4%, and 18.2%, respectively. BE had the highest plant growth-promoting effect compared to the other two biochar components, which was regardless of soil condition. In addition, the biomass, total volume, surface area, and number of maize root tips under BE amendment were significantly enhanced, particularly the fine roots (< 0.2 mm in diameter). And a strong positive correlation was observed between maize aboveground biomass and the total length of the fine roots. The results demonstrated that the water-soluble compounds present in biochar, in addition to the mineral nutrients and the washed biochar residue, dominate the plant growth promotion under both soil conditions.

     

HN1L promotes migration and invasion of breast cancer by up-regulating the expression of HMGB1

Recent reports showed that haematological and neurological expressed 1-like (HN1L) gene participated in tumorigenesis and tumour invasion. However, the expression and role of HN1L in breast cancer remain to be investigated. Here, bioinformatics, western blot and immunohistochemistry were used to detect the expression of HN1L in breast cancer. Wound healing, transwell assay, immunofluorescence assay and mass spectrum were used to explore the role and mechanism of HN1L on the migration and invasion of breast cancer, which was confirmed in vivo using a nude mice model. Results showed that HN1L was significantly over-expressed in breast cancer tissues, which was positively correlated with M metastasis of breast cancer patients. Silencing HN1L significantly inhibited the invasion and metastasis of breast cancer cells in vitro and lung metastasis in nude mice metastasis model of breast cancer. Mechanistically, HN1L interacted with HSPA9 and affected the expression of HMGB1, playing a key role in promoting the invasion and metastasis of breast cancer cell. These results suggested that HN1L was an appealing drug target for breast cancer.     

Contrasting responses of heterotrophic and autotrophic respiration to experimental warming in a winter annual‐dominated prairie

Understanding how soil respiration (Rs) and its source components respond to climate warming is crucial to improve model prediction of climate‐carbon (C) feedback. We conducted a manipulation experiment by warming and clipping in a prairie dominated by invasive winter annual Bromus japonicas in Southern Great Plains, USA. Infrared radiators were used to simulate climate warming by 3 °C and clipping was used to mimic yearly hay mowing. Heterotrophic respiration (Rh) was measured inside deep collars (70 cm deep) that excluded root growth, while total soil respiration (Rs) was measured inside surface collars (2–3 cm deep). Autotrophic respiration (Ra) was calculated by subtracting Rh from Rs. During 3 years of experiment from January 2010 to December 2012, warming had no significant effect on Rs. The neutral response of Rs to warming was due to compensatory effects of warming on Rh and Ra. Warming significantly (P < 0.05) stimulated Rh but decreased Ra. Clipping only marginally (P < 0.1) increased Ra in 2010 but had no effect on Rh. There were no significant interactive effects of warming and clipping on Rs or its components. Warming stimulated annual Rh by 22.0%, but decreased annual Ra by 29.0% across the 3 years. The decreased Ra was primarily associated with the warming‐induced decline of the winter annual productivity. Across the 3 years, warming increased Rh/Rs by 29.1% but clipping did not affect Rh/Rs. Our study highlights that climate warming may have contrasting effects on Rh and Ra in association with responses of plant productivity to warming.     

Arbuscular mycorrhizal fungi-enhanced resistance against Phytophthora sojae infection on soybean leaves is mediated by a network involving hydrogen peroxide, jasmonic acid, and the metabolism of carbon and nitrogen

The arbuscular mycorrhizal fungi (AMF) enhance the resistance to pathogen infection in host plant. However, it is unclear how the AMF are involved in the systemic acquired resistance of host plant against pathogen. Here, an experiment was carried out to clarify the role of the AMF in soybean’s defense against the infection from pathogen Phytophthora sojae. It was found that the AMF contributed to the resistance of soybean against Phytophthora sojae by the release of hydrogen peroxide and by the accumulation of jasmonic acid in response to pathogenic invasion. Furthermore, the trade of nitrogen (N) from the fungus for carbon from the host was accelerated in the AM symbiosis in the defense reaction, which was indicated by the increased soluble sugar level, NO content and enzyme activities involved in N metabolism in the AM symbiosis.     

Photosynthetic and Respiratory Acclimation to Experimental Warming for Four Species in a Tallgrass Prairie Ecosystem

Global temperature has been Increased by 0.6 ℃ over the past century and is predicted to Increase by 1.4-5.8 ℃ by the end of this century. It is unclear what impacts global warming will have on tallgrass species. In the present study, we examined leaf net photosynthetic rate （P.） and leaf respiration rate in darkness （Rd） of Aster erlcoldes （L.） Nesom, Ambrosia psllostachya DC., Helianthus mollis Lam., and Sorghastrum nutans （L.） Nash In response to experimental warming in a tallgrass prairie ecosystem of the Great Plains, USA, in the autumn （fall） of 2000 and through 2001. Warming has been Implemented with infrared heaters since 21 November 1999. The P. increased significantly In spring, decreased in early fall, and did not change in summer and late fall in the four species under warming compared with control. The Rd of the four species increased significantly until mid-summer and then did not change under warming. Measured temperature-response curves of P. showed that warming Increased the optimum temperature of P. （Topt） by 2.32 and 4.59 ℃ for H. mollis and S. nutans, respectively, in August, whereas there were no changes in May and September, and A. ericoldes and A. psllostachya also showed no changes in any of the 3 months. However, P. at optimum temperature （Popt） showed downregulation in September and no regulation in May and August for all four species. The temperature-response curves of Rd Illustrate that the temperature sensitivity of Rd, Q10, was lower in the warmed plots compared with the control plots, except for A. ericoides in August, whereas there were no changes In May and September for all four species. The results of the present study indicate that photosynthetic and respiratory acclimation varies with species and among seasons, occurring In the mid-growing season and not in the early and late growing seasons.     

Licochalcone A attenuates abdominal aortic aneurysm induced by angiotensin II via regulating the miR-181b/SIRT1/HO-1 signaling

Licochalcone A (LA), a chalcone derived from liquorice, exhibits multiple biological activities, including anti-oxidation and anti-inflammation. This study aimed to investigate the role and underlying mechanism of LA in the abdominal aortic aneurysm (AAA). AAA model was established by continuous infusion of 1000 ng/kg/min of angiotensin II (AngII) in ApoE ^-/- mice for 4 weeks. At 7 days before AngII administration, 5 mg/kg/day or 10 mg/kg/day of LA was intraperitoneally administered to mice and continued for 4 weeks. The characteristics and quantification of AAAs were determined in situ. Real-time PCR or western blot was used to measure mRNA or protein levels of matrix metalloproteinase 2 and matrix metalloproteinase 9; pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1β, and interleukin-6; apoptosis-related proteins Bax, Bcl-2, and active caspase-3; miR-181b; Sirtuin 1 (SIRT1); and heme oxygenase-1 (HO-1). Mouse-aorta-origin vascular smooth muscle (MOVAS) cells were used to confirm the involved pathways in vitro. We found LA administration dose-dependently reduced the incidence of AngII-induced AAA, aneurysm diameter enlargement, elastin degradation, matrix metalloproteinase production, pro-inflammatory cytokines and miR-181b expression, and vascular smooth muscle cell apoptosis. It elevated SIRT1 and HO-1 expression that was suppressed by AngII. AngII enhanced miR-181b but reduced SIRT1 and HO-1 expression in MOVAS cells. In AngII-stimulated MOVAS cells, downregulation of miR-181b significantly upregulated the expression of SIRT1 and HO-1, the effect of which was abrogated by SIRT1 siRNA. Collectively, LA could attenuate AngII-induced AAA by modulating the miR-181b/SIRT1/HO-1 signaling. LA might be a potential medical therapy for small AAA.     

microRNA-338-3p promotes ox-LDL-induced endothelial cell injury through targeting BAMBI and activating TGF-β/Smad pathway

microRNAs (miRNAs) have been revealed to participate in the pathological process of atherosclerosis (AS). However, the exact role of miR-338-3p, a target miRNA of BMP and activin membrane-bound inhibitor (BAMBI), and its possible molecular mechanism in AS remain unidentified. In this study, we found that BAMBI was significantly decreased, whereas miR-338-3p increased in patients with AS and oxidized low-density lipoprotein (ox-LDL)-induced HUVEC cells. Furthermore, overexpression of miR-338-3p significantly decreased cell viability and elevated cell apoptosis, whereas its inhibition significantly promoted cell viability and inhibited cell apoptosis in ox-LDL-induced HUVEC cells. Moreover, miR-338-3p overexpression increased TGF-β/Smad pathway activation in ox-LDL-induced HUVEC cells. A dual-luciferase reporter assay confirmed the direct interaction between miR-338-3p and the 3′-untranslated region of BAMBI messenger RNA. Furthermore, the suppression of BAMBI ameliorated the effect of miR-338-3p inhibition against ox-LDL-induced HUVEC cell injury. In conclusion, our study thus suggests that miR-338-3p promoted ox-LDL-induced HUVEC cell injury by targeting BAMBI and activating the TGF-β/Smad pathway, which may provide a novel and promising therapeutic target for AS.