溶磷菌和固氮菌溶解磷矿粉时的互作效应

采用4株溶磷菌（Lx81、Dm84、Jm92、Lx191）、和3株固氮菌（ChW5、ChW6、ChO6）单独和混合接种后测定培养液有效磷含量、pH值及总有机酸含量的方法,研究溶磷菌和固氮菌溶解磷矿粉时的互作效应。结果表明,相对于单独接种溶磷菌：Lx81与3株固氮菌分别混合培养能提高磷矿粉的溶解能力,4株溶磷菌与ChW6,Lx81、Dm84、Lx191与Ch06分别混合培养及Jm92＋ChW5组合溶磷量极显著增加（P〈0．01）;Dm84＋ChW5、Lxl91＋ChW5、Jm92＋Ch06组合的溶磷量下降（P〈0．01）。除Lx81＋ChW6、Lx81＋Ch06培养液pH值降低外,混合培养的其它组合培养液pH值均较单独接种溶磷菌时升高。有机酸测定结果表明,Lx81、Jm92与ChW5、Ch06分别混合培养、ChW6＋Lx81组合有机酸含量升高（P〈0．01）,其它7种组合的有机酸含量均较单独接种溶磷菌的值下降（P〈0．01）。溶磷菌和固氮菌单菌培养时溶磷量与pH值、溶磷量与总有机酸含量及pH值与总有机酸含量之间呈现线性相关;Dm84、Lx191与3株固氮菌分别混合培养溶磷量与pH值之间、Lx81与3株固氮菌分别混合培养溶磷量与总有机酸含量之间呈现线性相关,其它组合的溶磷量与pH值、总有机酸含量间没有相关性。溶磷菌和固氮菌混合培养对溶解磷矿粉既有协同作用也有拮抗作用。     

Cd胁迫对紫花苜蓿种子发芽及幼苗生理生化特性的影响

以‘甘农3号’紫花苜蓿(Medicago sativa L.cv.‘Gannong 3’)品种为试验材料,研究不同浓度Cd胁迫对紫花苜蓿种子萌发及幼苗生理生化特性的影响。结果显示:(1)Cd胁迫显著抑制紫花苜蓿种子萌发及幼苗生长,种子发芽势、发芽率及幼苗的胚芽长、胚根长和干重均随着Cd处理浓度提高显著降低,且对发芽势的抑制作用大于发芽率,对胚根生长的抑制作用大于胚芽。(2)Cd胁迫第4d时,萌发种子中蛋白水解酶的活性受到显著抑制,可溶性蛋白和可溶性糖含量显著降低。(3)Cd胁迫第10d时,随着Cd胁迫浓度的增加,苜蓿幼苗的超氧化物歧化酶(SOD)、抗坏血酸过氧化物酶(APX)、愈创木酚过氧化物酶(GPX)活性均先升高后降低,过氧化氢酶(CAT)活性持续下降,超氧阴离子自由基产生速率、H2O2含量和丙二醛(MDA)含量均显著增加。研究表明,低浓度Cd胁迫下,苜蓿幼苗抗氧化系统清除活性氧的能力上升,高浓度Cd胁迫下,苜蓿幼苗抗氧化系统活性下降,膜脂过氧化程度加剧,活性氧的过量积累是Cd伤害苜蓿幼苗和其生物量下降的主要原因。     

Genome-wide signatures of the geographic expansion and breeding of soybean

Soybean is a leguminous crop that provides oil and protein. Exploring the genomic signatures of soybean evolution is crucial for breeding varieties with improved adaptability to environmental extremes. We analyzed the genome sequences of 2,214 soybeans and proposed a soybean evolutionary route, i.e., the expansion of annual wild soybean (Glycine soja Sieb. & Zucc.) from southern China and its domestication in central China, followed by the expansion and local breeding selection of its landraces (G. max (L.) Merr.). We observed that the genetic introgression in soybean landraces was mostly derived from sympatric rather than allopatric wild populations during the geographic expansion. Soybean expansion and breeding were accompanied by the positive selection of flowering time genes, including GmSPA3c. Our study sheds light on the evolutionary history of soybean and provides valuable genetic resources for its future breeding.

     

Macrophages largely contribute to heterologous anti‐Propionibacterium acnes antibody‐mediated protection from Actinobacillus pleuropneumoniae infection in mice

Actinobacillus pleuropneumoniae is the causative agent of acute and chronic pleuropneumonia. Propionibacterium acnes is a facultative anaerobic gram‐positive corynebacterium. We have previously found that anti‐P. acnes antibodies can prevent A. pleuropneumoniae infections in mice. To investigate the role of macrophages in this process, affinity‐purified anti‐P. acnes IgG and anti‐A. pleuropneumoniae IgG were used in opsonophagocytosis assays. Additionally, the efficacy of passive immunization with P. acnes serum against A. pleuropneumoniae was tested in macrophage‐depleted mice. It was found that anti‐P. acnes IgG had an effect similar to that of anti‐A. pleuropneumoniae IgG (P > 0.05), which significantly promotes phagocytosis of A. pleuropneumoniae by macrophages (P < 0.01). It was also demonstrated that, after passive immunization with anti‐P. acnes serum, macrophage‐replete mice had the highest survival rate (90%), whereas the survival rate of macrophage‐depleted mice was only 40% (P < 0.05). However, macrophage‐depleted mice that had been passively immunized with naïve serum had the lowest survival rate (20%), this rate being lower than that of macrophage‐replete mice that had been passively immunized with naïve serum. Overall, anti‐P. acnes antibodies did not prevent A. pleuropneumoniae infection under conditions of macrophage depletion (P > 0.05). Furthermore, in mice that had been passively immunized with anti‐P. acnes serum, macrophage depletion resulted in a greater A. pleuropneumoniae burden and more severe pathological features of pneumonia in lung tissues than occurred in macrophage‐replete mice. It was concluded that macrophages are essential for the process by which anti‐P. acnes antibody prevents A. pleuropneumoniae infection in mice.     

Bronchial epithelial DNA methyltransferase 3b dampens pulmonary immune responses during Pseudomonas aeruginosa infection

DNA methyltransferase (Dnmt)3b mediates de novo DNA methylation and modulation of Dnmt3b in respiratory epithelial cells has been shown to affect the expression of multiple genes. Respiratory epithelial cells provide a first line of defense against pulmonary pathogens and play a crucial role in the immune response during pneumonia caused by Pseudomonas (P.) aeruginosa, a gram-negative bacterium that expresses flagellin as an important virulence factor. We here sought to determine the role of Dntm3b in respiratory epithelial cells in immune responses elicited by P. aeruginosa. DNMT3B expression was reduced in human bronchial epithelial (BEAS-2B) cells as well as in primary human and mouse bronchial epithelial cells grown in air liquid interface upon exposure to P. aeruginosa (PAK). Dnmt3b deficient human bronchial epithelial (BEAS-2B) cells produced more CXCL1, CXCL8 and CCL20 than control cells when stimulated with PAK, flagellin-deficient PAK (PAKflic) or flagellin. Dnmt3b deficiency reduced DNA methylation at exon 1 of CXCL1 and enhanced NF-ĸB p65 binding to the CXCL1 promoter. Mice with bronchial epithelial Dntm3b deficiency showed increased Cxcl1 mRNA expression in bronchial epithelium and CXCL1 protein release in the airways during pneumonia caused by PAK, which was associated with enhanced neutrophil recruitment and accelerated bacterial clearance; bronchial epithelial Dnmt3b deficiency did not modify responses during pneumonia caused by PAKflic or Klebsiella pneumoniae (an un-flagellated gram-negative bacterium). Dnmt3b deficiency in type II alveolar epithelial cells did not affect mouse pulmonary defense against PAK infection. These results suggest that bronchial epithelial Dnmt3b impairs host defense during Pseudomonas induced pneumonia, at least in part, by dampening mucosal responses to flagellin.     

紫花苜蓿对牛角花齿蓟马为害的光合生理响应

为了探索紫花(Medicago sativa L.)苜蓿对优势种害虫——牛角花齿蓟马(Odontothrips loti Haliday)为害的光合生理响应机制,揭示苜蓿对牛角花齿蓟马为害的补偿机制,以抗蓟马苜蓿无性系R-1和感蓟马苜蓿无性系I-1为材料,测定不同虫口密度牛角花齿蓟马为害后R-1、I-1无性系气体交换参数、叶绿素荧光诱导动力学参数的变化。结果表明:随着牛角花齿蓟马虫口密度的增加,R-1无性系叶绿素含量先升高后降低,I-1无性系叶绿素含量降低,R-1、I-1无性系的净光合速率(Pn)和水分利用效率(WUE)降低,胞间CO2浓度(Ci)、气孔导度(Gs)和蒸腾速率(Tr)升高;在相同虫口密度下,R-1无性系的叶绿素含量、Pn、WUE均高于I-1无性系。随着虫口密度的增加,R-1、I-1无性系的初始荧光(F0)升高,PSⅡ实际光合效率(ФPSⅡ)、非光化学淬灭系数(NPQ)、光化学淬灭系数(q P)、PSⅡ潜在活性(Fv/F0)和PSⅡ原初光能转化效率(Fv/Fm)均降低;在相同虫口密度下,R-1无性系的F0低于I-1无性系,R-1无性系的ФPSⅡ、q P、Fv/F0和Fv/Fm均高于I-1无性系。从各个指标的变化幅度来看,随着虫口密度的增加,R-1无性系气体交换参数和绿素荧光动力学参数的增幅、降幅均小于I-1无性系。说明牛角花齿蓟马为害造成了紫花苜蓿PSⅡ反应中心受损,使得紫花苜蓿对光能的利用能力下降,光合效率降低。但在低虫口密度(1、3头/枝条)下,R-1无性系具有较高的光合效率,光合补偿效应显著大于I-1无性系,说明R-1无性系对牛角花齿蓟马为害具有较强的抗性。     

NO对盐胁迫下苜蓿根系生长抑制及氧化损伤的缓解效应

以"甘农4号"苜蓿品种为材料,采用水培法,用NO供体硝普钠(SNP)、硝普钠类似物亚铁氰化钠(不产生NO)、NO特异清除剂c-PTIO、一氧化氮合酶(NOS)活性抑制剂N-硝基-L-精氨酸甲脂(L-NAME)、硝酸还原酶(NR)活性抑制剂钨酸盐处理苜蓿植株,研究NO对盐胁迫下苜蓿幼苗根系生长、根系活力、根系中渗透调节物质、膜脂过氧化、活性氧含量及抗氧化酶活性等的影响,探讨NO调控苜蓿幼苗根系耐盐性的生理机制。结果表明:盐胁迫下SNP处理提高了根系活力,促进了苜蓿幼苗根系生长,降低游离脯氨酸含量,促进可溶性蛋白含量增加;增强超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、愈创木酚过氧化物酶(GPX)、抗坏血酸过氧化物酶(APX)和谷胱甘肽还原酶(GR)活性,提高还原型抗坏血酸(As A)和还原型谷胱甘肽(GSH)含量,降低过氧化氢(H2O2)、羟自由基(OH·)含量、超氧阴离子(O·-2)产生速率和膜脂过氧化产物丙二醛(MDA)含量;同时,SNP处理显著促进了苜蓿幼苗根系内源NO的积累。NO供体SNP的类似物亚铁氰化钠对盐胁迫下苜蓿根系各项生理生化指标无明显影响;盐胁迫下添加c-PTIO、L-NAME和钨酸盐进一步降低了苜蓿幼苗根系活力和根系生长,抑制了根系抗氧化系统活性,加剧了根系膜脂过氧化作用,降低了内源NO积累,添加SNP则能缓解该抑制效应;表明外源SNP处理能明显缓解盐胁迫对苜蓿幼苗根系生长的抑制和氧化损伤,且通过NOS和NR途径产生的内源NO也可能在苜蓿根系适应盐胁迫的调节中起关键作用;该研究结果为苜蓿耐盐机制及NO在苜蓿耐盐育种、化学调控和盐碱地栽培利用等提供了理论依据。