蓖麻株高性状主基因+多基因遗传分析

本研究选用蓖麻YC2×YF1高、矮秆组合的2组6世代群体(P1、P2、F1、B1、B2和F2),对株高性状进行了主基因+多基因混合遗传模型分析。结果表明,蓖麻株高受1对主基因和多基因共同控制。2组群体在B1、B2和F2三个分离世代中主基因遗传率分别为37.05%/49.57%、30.51%/34.48%和43.98%/43.64%;主穗位高和主茎节数均受2对主基因和多基因共同控制,且主基因的互作效应显性效应加性效应。3个分离世代中,2组群体主穗位高主基因遗传率分别为67.91%/92.72%、86.89%/92.13%和60.18%/66.87%,主茎节数主基因遗传率分别为91.83%/91.50%、35.22%/63.37%和85.76%/94.58%。主茎节长由多基因控制,遗传率分别为47.64%/47.64%、38.87%/38.87%和25.25%/52.71%。以上遗传模式决定了蓖麻杂种后代株高、主穗位高和主茎节长的正向超亲遗传,而主茎节数则倾向于低值亲本。因此,主穗位高和主茎节数可以作为株高的早期间接选择指标。     

高温预处理玉米秸秆条件的优化

对玉米秸秆高温预处理条件进行优化,以降低还原糖损失率和提高灰分去除率为目的,探讨了高温预处理时料液比、蒸煮温度、蒸煮时间对还原糖得率的影响。通过采用单因素多水平试验方法得到最优预处理条件为料液比1∶7,蒸煮温度118℃,蒸煮时间0.5 h。在此最优条件下,预处理后的秸秆还原糖损失率为1.86%,灰分去除率为35.2%。     

生化和ISSR分子标记在黑木耳品种鉴定中的应用

以生产收集的24个黑木耳栽培菌株为试材,采用拮抗、酯酶同工酶及ISSR分子标记技术对其进行分类鉴定和遗传多样性分析。结果表明:酯酶同工酶酶谱显示24个黑木耳菌株共扩增出11条迁移率不同的酶带,聚类分析表明当遗传系数为0.74时,将24个黑木耳菌株分为两大类;通过ISSR分子标记共扩增出67条清晰的DNA多态片段,大小介于0.2～2.0 kb,聚类分析表明当遗传系数为0.85时,将24个菌株分为两大类,聚类分析结果与拮抗试验结果基本一致。该研究为黑木耳的菌株选择及遗传育种提供了参考依据。     

枸杞玻璃化组培苗恢复技术

以枸杞不同程度玻璃化组培苗为试材,采用组织培养法,研究了不同基本培养基、外源添加物、添加聚丙烯酰胺、改变培养条件及玻璃化苗脱水处理在玻璃化组培苗恢复中的作用,探索出最佳的枸杞玻璃化组培苗恢复方法。结果表明:1/2MS+6-BA 0.5mg·L^-1+活性炭0.5g·L^-1为枸杞轻度玻璃化苗恢复最佳培养基,适宜枸杞中度玻璃化苗恢复培养基为1/4MS+6-BA 0.5mg·L^-1+活性炭1.0g·L^-1。当添加聚丙烯酰胺8、16g·L^-1,枸杞轻度、中度玻璃化苗恢复率均达到最高,聚丙烯酰胺对枸杞玻璃化的组培苗有明显的逆转效果,逆转后的组培苗生长良好。经过脱水处理后,玻璃化苗明显得到恢复。脱水2d轻度玻璃化苗的恢复率可达77.61%。随着脱水的天数增加,枸杞中度玻璃化苗恢复率逐渐提高,当脱水天数达3d时,恢复率最高达71.24%。培养期间增强封口膜的透气性和光照强度能有效提高枸杞玻璃化苗恢复率。     

薄壳山核桃品种波尼的引种表现与栽培技术

2013年引进薄壳山核桃品种波尼在山东省济宁市汶上试栽,经多年观察表明,该品种为早熟品种,平均单果重10. 25g;早实丰产,抗旱耐涝,适应性强,果实生长期145～165天,成熟期9月底～10月初。栽培时用科尔比、威奇塔、金华等做授粉树。     

果蝇毛锤角细蜂对黑腹果蝇蛹不同龄期的选择性

黑腹果蝇Drosophila melanogaster Meigen是浆果类水果的果实害虫之一,对葡萄果实为害严重。毛锤角细蜂Trichopria drosophilae是黑腹果蝇的蛹寄生蜂之一。本文在温度26℃、相对湿度50%、光周期14L:10D的室内条件下,研究了毛锤角细蜂对不同日龄黑腹果蝇蛹的选择性。结果表明:毛锤角细蜂可寄生黑腹果蝇各日龄的蛹,但偏爱寄生预蛹。在寄主预蛹时,毛锤角细蜂的出蜂量、寄生率和选择系数分别为14.00头、35%和0.13,均显著高于1~3日龄蛹;不同日龄的黑腹果蝇蛹对毛锤角细蜂后代发育历期和雌蜂比没有显著影响。综上所述,黑腹果蝇的预蛹是毛锤角细蜂寄生的最佳时期。以黑腹果蝇为寄主时,研究毛锤角细蜂的寄生规律对于黑腹果蝇及其他果蝇的生物防治具有重要的指导意义。     

采用胚挽救获得Ogura CMS甘蓝与甘蓝型油菜的种间杂种

为将甘蓝型油菜细胞质雄性不育系(Ogura CMS)的恢复基因转至甘蓝Ogura CMS材料上,以6份甘蓝Ogura CMS材料为母本,以含恢复基因的甘蓝型油菜为父本,人工杂交结合胚挽救培养,研究取材时期、培养基成分和杂交组合对胚珠成苗的影响,同时对胚挽救培养获得的植株是否为真实F1杂种进行鉴定。结果发现,胚珠培养以剥蕾授粉后16d取材时胚珠成苗数最多,成苗率为4.56%;培养基以MS+GA 0.1 mg·L^-1+NAA 0.1 mg·L^-1+0.5%水解酪蛋白(CH)+0.5%活性炭(AC)成苗效果最好,成苗率高达6.24%;M09CMS×RFO-46组合成苗数最多,成苗率为5.96%。67株胚挽救培养得到的植株经流式细胞仪、SSR分子标记和形态学鉴定,得出65株为真杂种,真杂种率高达97%。     

葡萄叶片衰老过程中不同光质对其光合和叶绿体超微结构的影响

以栽植于日光温室中适宜延迟栽培的‘贝达’砧‘意大利’葡萄为试材,自2013年8月1日始至落叶(2014年1月31日)止每天分别进行红光和蓝光不同光质延长光照至24:00补光处理,以不补光作为对照,研究不同光质补光处理对葡萄叶片衰老过程中叶片的外观形态特征、叶绿素含量、净光合速率、F_v/F_m、可溶性蛋白质含量和叶绿体超微结构的影响,为叶片抗衰老技术的研发提供理论依据。研究结果表明:补充红光显著提高了叶片的叶绿素含量、净光合速率、F_v/F_m值和可溶性蛋白质含量,叶绿体基粒片层排列整齐有序,明显减缓了叶绿体超微结构的解体,显著延缓叶片衰老;补充蓝光处理前期显著降低了叶片的叶绿素含量、净光合速率、F_v/F_m值和可溶性蛋白质含量,破坏了叶绿体的超微结构,加速了植株的衰老进程;但在叶片衰老后期,叶绿素含量、净光合速率、F_v/F_m值和可溶性蛋白质含量逐渐高于对照,并且叶绿体的基粒片层比对照排列整齐有序,在一定程度上延缓了叶片衰老。补充蓝光处理的叶片可溶性蛋白质含量一直显著高于补充红光和对照。综上,补充红光处理有效延缓了叶片衰老进程,延长了叶片的生理功能期。     

Protective effect of Huangqi injection combined with puerarin injection on myocardium of type 2 diabetes mice

AIM:To investigate the effect of Huangqi injection combined with puerarin injection on the myocardium of the mice with type 2 diabetes. METHODS:Diabetic KKAy mice were randomly divided into model group and treatment group (Huangqi injection combined with puerarin injection). The male KKAy mice of the same age were used as control group. All mice were sacrificed at 21, 24 and 28 weeks. Morphological changes of the myocardium were observed by HE staining. Apoptosis of the cardiomyocytes was measured by TUNEL staining. The mRNA levels of glucose-regulated protein 78(GRP78), C/EBP hoinologous protein (CHOP) and p53 up-regulated modulator of apoptosis (PUMA) were detected by real-time PCR, and the protein levels of GRP78, CHOP, PUMA, caspase-3, cleaved caspase-3, caspase-9, cleaved caspase-9, poly(ADP-ribose) polymerase (PARP) and cleaved PARP were determined by Western blot. RESULTS:Cardiomyocyte hypertrophy, partly dissolved sarcoplasm and necrosis were observed in model group, and these lesion were alleviated in treatment group. Obvious increased apoptosis in model group and significantly decreased apoptosis of cardiomyocytes in treatment group was observed (P<0.05). At 21, 24 and 28 weeks, the mRNA and protein levels of GRP78, CHOP and PUMA and the protein levels of cleaved caspase-3, cleaved caspase-9 and cleaved PARP in model group were increased significantly as compared with control group (P<0.01), and these in treated group were decreased compared with model group. CONCLUSION:Huangqi injection combined with puerarin injection has cardioprotective effects on type 2 diabetes mice and its mechanism of the action was implemented via inhibiting the activation of endoplasmic reticulum stress and caspase pathway, thus resulting in suppressed apoptosis.     

Role of ghrelin in cell protection by up-regulating HSP70 through ERK1/2 signaling pathway in PC12 cells

AIM:To study the role of ghrelin in cell protection by up-regulating heat shock protein 70 (HSP70) and inhibiting apoptosis induced by oxidative stress through extracellular regulated protein kinases 1/2 (ERK1/2) signaling pathway in the PC12 cells. METHODS:Sodium nitoprusside (SNP) was used to induce oxidative stress injury in the PC12 cells. The cultured PC12 cells were divided into SNP-injured group (incubated with SNP at 0.5 mmol/L for 6, 12, 18 and 24 h), ghrelin pretreatment group (ghrelin at 100 nmol/L was given 30 min before adding SNP); HSP70 inhibitor group (quercetin at 10 μmol/L was added 60 min before ghrelin treatment), ERK inhibitor group (ERK 1/2 inhibitor PD98059 was added 60 min before ghrelin treatment) and control group (added same amount of culture medium only). The apoptotic rate was detected by flow cytometry. The protein expression was determined by Western blot and immunocytochemistry. RESULTS:Compared with control group, the apoptotic rate of PC12 cells in SNP-injured group was significantly increased (P<0.05). Compared with SNP-injured group, ghrelin (100 nmol/L) pretreatment significantly inhibited SNP-induced apoptosis of PC12 cells (P<0.05), and significantly up-regulated the protein expression of HSP70 (P<0.05). Time-effect analysis showed that ghrelin had the most significant effect at 18 h after SNP injury. Quercetin, an inhibitor of HSP 70, significantly reduced the anti-apoptotic effect of ghrelin (P<0.05). Ghrelin pretreatment promoted the phosphorylation of ERK1/2. ERK1/2 inhibitor PD98059 significantly inhibited the effects of ghrelin on up-regulation of HSP70 expression (P<0.05). CONCLUSION:Ghrelin upregulates the expression of HSP70 and inhibits the apoptosis in the PC12 cells induced by oxidative stress by promoting the phosphorylation of ERK1/2.