Allelochemical p-hydroxybenzoic acid inhibits root growth via regulating ROS accumulation in cucumber(Cucumis sativus L.)

Allelopathy is prevalent in agricultural ecosystems and mediated by plant-derived secondary metabolites(allelochemicals).Allelochemicals are released by donor plants and affect the root growth and development of receptor plants.Allelopathy is responsible for the continuous cropping obstacles in cucumber(Cucumis sativus L.).p-Hydroxybenzoic acid(pHBA),an autotoxin from root exudates of cucumber,has been proposed to be an important allelopathic chemical.However,the molecular mechanism by which pHBA affect root growth and development in cucumber is unknown.Here,we found that pHBA treatment suppressed root growth of cucumber by reducing the meristem activity and cell length.This root growth defect is caused by reduced reactive oxygen species(ROS)accumulation in root tips.After pHBA treatment,the expression levels of several ROS-scavenging-related genes were increased,including peroxidase(POD),catalase(CAT)and metallothionein(MT).Moreover,exogenously application of salicylhydroxamate(SHAM),a peroxidase inhibitor,can partially restore the pHBA treatment induced root growth inhibition.Furthermore,we found that there is natural variation for the inhibitory effect of pHBA on root growth.We also showed that pHBA treatment could maintain higher level of ROS accumulated in the pHBA less sensitive cucumber than that in the pHBA-sensitive cucumber.These results suggest that pHBA inhibits root growth by reducing root tip ROS level in cucumber.

普通生物炭和酸改性生物炭对盐渍土入渗、蒸发过程的影响

探究生物炭以及改性生物炭对盐渍土入渗、蒸发能力以及含水率、pH、含盐量的影响。通过室内土柱试验,研究了2种生物炭(普通小麦秸秆生物炭A、磷酸改性生物炭B)3个添加量(2%、4%、8%)共计6个试验组以及1个对照组(CK、A1、A2、A3、B1、B2、B3)条件下,盐渍土入渗、蒸发过程中湿润峰运移、累积入渗量、蒸发量、含水率、pH以及含盐量的动态变化。结果表明,①在入渗阶段,观测累积入渗量以及湿润峰运移距离两项指标,发现添加生物炭和改性生物炭均能够有效促进土壤水分入渗,且添加量越多,促进效果越明显。②添加改性生物炭更能增大土壤入渗结束1 d后的土壤含水率,且对土壤pH的改良效果更好,B3处理显著增大了0~15 cm土层土壤的含盐量,A1处理显著降低了15~30 cm土层土壤的含盐量。③各处理对土壤蒸发的影响较小,仅在A3处理下对土壤蒸发产生了抑制。添加4%的改性生物炭能够有效降低土壤的pH,促进土壤水分的入渗,对改良盐渍土具有良好作用。

衰老蛋白p66^(Shc)在成年小鼠心肌组织修复中的研究

本研究组前期研究显示衰老蛋白p66^(Shc)在新生小鼠心肌再生的过程中发挥着重要的作用,p66^(Shc)缺失会导致新生小鼠受损心肌再生能力减弱。本文旨在探讨p66^(Shc)蛋白在成年小鼠心肌梗死(简称心梗)后心肌损伤修复中的作用,以期为心梗后心肌损伤治疗提供新的靶点。通过前降支结扎手术构建成年野生型(WT)和p66^(Shc)敲除(KO)小鼠心梗模型,比较分析两种小鼠心梗术后的生存率和心重体重比,用Masson染色检测受损心肌瘢痕化面积,用麦胚凝集素(wheat germ agglutinin, WGA)染色测定小鼠心梗后心肌细胞面积,用TUNEL染色检测心肌细胞的凋亡程度,用Western blotting检测心肌肥厚常用标志物脑利尿钠肽(brain natriuretic peptide, BNP)的表达变化。结果显示,与野生型小鼠相比,p66^(Shc)KO小鼠心梗术后的生存率、心肌瘢痕化面积、心肌细胞凋亡、心重体重比无显著差异,而BNP蛋白表达水平下调。以上结果提示,与新生小鼠不同,衰老蛋白p66^(Shc)的缺失对成年小鼠心梗后心肌损伤修复没有显著作用。