杨树对叶锈病的生物化学抗性机制研究
|
摘要
杨树是一种重要的生态和商品林树种,由落叶松-杨栅锈菌所引起的杨树叶锈病是一种重大的杨树叶部病害。国内外研究表明,抗病性品种的应用能达到持久防治杨树叶锈病的作用。本研究从不同杨树品种与不同落叶松-杨栅锈菌生理小种的互作关系出发,对该互作过程中杨树叶片组织中的活性氧爆发、相关酶活性动态变化、组织结构中的木质素与寄主抗病性的关系进行研究,并探讨该互作过程中PCD的发生机制,以期为杨树叶锈病发生的分子机制和选育抗病杨树品种提供科学依据。研究结果表明:
1、不同的杨树品种(种)接种落叶松-杨栅锈菌后ROS变化幅度差异显著。O_2~-产生速率、H_2O_2含量分别在0.5d、1d时迅速上升,与对应对照相比,各品种ROS上升的幅度在各自病程中均为最高点。在感病品种中ROS变化往往只出现一个峰值,而在抗病品种中常常出现2~3个峰值,且抗锈性越高,出现第二个峰值的时间越早,ROS值也越高。整个病程中免疫、抗病组合寄主的ROS波动速度及幅度明显大于感病品种。
2、杨树接种落叶松-杨栅锈菌后POD、SOD、CAT活性一直处于一个动态变化的过程,彼此间相互协同控制。SOD活性与杨树寄主抗病性呈负相关。POD活性前期变化不显著,后期与抗病性呈负相关。各品种接种后CAT活性0.5 d迅速上升,1 d后下降,3~5 d时出现高峰,表现为抗锈性越强,CAT活性越低。
3、免疫、高抗品种杨树受松-杨栅锈菌侵染后PAL活性上升速度快、强度大,各组合与对应对照的比值间存在显著差异。几丁质酶活性与杨树品种的抗病性基本呈正相关。抗病品种出现2~3次高峰,且在与对应对照的比值中,免疫品种同其他品种间存在显著差异,而其余品种间差异较小。
4、杨树与落叶松-杨栅锈菌互作病程中,1d~2d时不亲合组合叶片组织内就有少量木质素的积累,3d时积累比较明显。在亲和组合和健康对照中叶片木质素的积累非常少,而高抗品种中积累较多。木质素的积累与杨树抗锈性无明显的相关性。
5、杨树叶片切片后经DAPI染色在荧光显微镜下观察细胞核发出强烈的蓝光,不同品种杨树健康叶片的细胞核呈圆形或近圆形。抗病品种川杨受落叶松-杨栅锈菌侵染后有HR现象,且表现出明显的PCD特征,接种0.5d时细胞核开始发生变化,3~4 d时细胞核裂解,7d后细胞核消失。感病品种太白杨接种后出现HR但不属于PCD范畴。
Poplar is an important ecological and commercial forest tree species. Leaf rust is a major leaf disease, which is caused by Melampsora larici-populina Kleb. Research of domestic and foreign experts showed that the application of disease resistant species could be used to control the poplar leaf rust. The interaction between different poplar species and different Melampsora larici-populina Kleb. races was studied firstly in this paper. The relationship in this interaction between outbreak of reactive oxygen, dynamic changes of related enzyme activity and lignin content in the tissue structure in poplar leaf tissues and the host disease resistance was studied. Then PCD mechanism of the host after inoculated with Melampsora larici-populina Kleb. was discussed to provide scientific basis for the molecular mechanism of poplar leaf rust and poplar disease resistance varities screening .The conclusions showed that:
1、There were significantly differences on the variation amplitude of ROS in the different poplar varieties (species) after inoculated with Melampsora larici-populina Kleb.The production rate of O_2~- and the content of H2O2 respectively rapidly increased in 0.5 d and 1 d, furthermore ROS of each varity was the highest in it’s pathogene process compared with the CK. The change of ROS in susceptible species often appeared one peak and 2 to 3 peaks in the resistant ones. Moreover, the higher resistance to rust, the sooner occuring of second peak,and the higher of ROS value. ROS was fluctuatedly changed throughout the infection process,and the rate of ROS fluctuation rate immune and resistance in the susceptible varieties was higher than susceptible.
2、The activity of POD, SOD and CAT had a dynamic change all the time after poplar inoculated with Melampsora larici-populina Kleb., and they were cooperative controled by each other. The activity of SOD was negatively correlated with the poplar resistance. The POD activity did not change significantly in early period after inoculation, but it had negative correlation with disease resistance later. The CAT activity was highly increased in 0.5 d ,then decreased in 1 d,moreover appeared one peak in 3 d to 5 d.The higher resistance to rust the lower CAT activity.
3、The PAL activity increased rapidly and had stronger strength in the host of immune and resistance species after inoculated with Melampsora larici-populina Kleb. There were significant differences in the ration of PAL activity in each combination to the corresponding controls. The chitinase activity was positively correlated with poplar resistance basically. There were 2~3 times of peaks in the resistant poplar varieties. In the ratio with the corresponding controlls, there was significantly difference between immune and others species, but little differences in others.
4、In the pathogene process between poplar and Melampsora larici-populina Kleb.,there was very little accumulation of lignin in 1 d to 2 d in the leave tissue of incompatible combinations and comparatively obvious accumulation in 3 d. But lignin almost had no accumulation in the compatible one and healthy control, while more accumulation in highly resistant poplar varieties. There was no correlation between the accumucation of lignin and poplar rust resistance.
5、Using DAPI stain after slicing the poplar leaves ,there was a strong blue light in mucli under the fluorescence microscope. The nucleolus were round or nearly round in the healthy leaves of different poplar varieties. There was HR phenomena and significantly change of PCD in P. szechuanica after inoculated with Melampsora larici-populina Kleb. The nuclei began to change in 0.5d after inoculation, then cracked in 5 d, disappeared in 7 d at last. However we found HR phenomenon after the inoculation of Populus purdomii,but it did not belong to PCD process.
1、不同的杨树品种(种)接种落叶松-杨栅锈菌后ROS变化幅度差异显著。O_2~-产生速率、H_2O_2含量分别在0.5d、1d时迅速上升,与对应对照相比,各品种ROS上升的幅度在各自病程中均为最高点。在感病品种中ROS变化往往只出现一个峰值,而在抗病品种中常常出现2~3个峰值,且抗锈性越高,出现第二个峰值的时间越早,ROS值也越高。整个病程中免疫、抗病组合寄主的ROS波动速度及幅度明显大于感病品种。
2、杨树接种落叶松-杨栅锈菌后POD、SOD、CAT活性一直处于一个动态变化的过程,彼此间相互协同控制。SOD活性与杨树寄主抗病性呈负相关。POD活性前期变化不显著,后期与抗病性呈负相关。各品种接种后CAT活性0.5 d迅速上升,1 d后下降,3~5 d时出现高峰,表现为抗锈性越强,CAT活性越低。
3、免疫、高抗品种杨树受松-杨栅锈菌侵染后PAL活性上升速度快、强度大,各组合与对应对照的比值间存在显著差异。几丁质酶活性与杨树品种的抗病性基本呈正相关。抗病品种出现2~3次高峰,且在与对应对照的比值中,免疫品种同其他品种间存在显著差异,而其余品种间差异较小。
4、杨树与落叶松-杨栅锈菌互作病程中,1d~2d时不亲合组合叶片组织内就有少量木质素的积累,3d时积累比较明显。在亲和组合和健康对照中叶片木质素的积累非常少,而高抗品种中积累较多。木质素的积累与杨树抗锈性无明显的相关性。
5、杨树叶片切片后经DAPI染色在荧光显微镜下观察细胞核发出强烈的蓝光,不同品种杨树健康叶片的细胞核呈圆形或近圆形。抗病品种川杨受落叶松-杨栅锈菌侵染后有HR现象,且表现出明显的PCD特征,接种0.5d时细胞核开始发生变化,3~4 d时细胞核裂解,7d后细胞核消失。感病品种太白杨接种后出现HR但不属于PCD范畴。
Poplar is an important ecological and commercial forest tree species. Leaf rust is a major leaf disease, which is caused by Melampsora larici-populina Kleb. Research of domestic and foreign experts showed that the application of disease resistant species could be used to control the poplar leaf rust. The interaction between different poplar species and different Melampsora larici-populina Kleb. races was studied firstly in this paper. The relationship in this interaction between outbreak of reactive oxygen, dynamic changes of related enzyme activity and lignin content in the tissue structure in poplar leaf tissues and the host disease resistance was studied. Then PCD mechanism of the host after inoculated with Melampsora larici-populina Kleb. was discussed to provide scientific basis for the molecular mechanism of poplar leaf rust and poplar disease resistance varities screening .The conclusions showed that:
1、There were significantly differences on the variation amplitude of ROS in the different poplar varieties (species) after inoculated with Melampsora larici-populina Kleb.The production rate of O_2~- and the content of H2O2 respectively rapidly increased in 0.5 d and 1 d, furthermore ROS of each varity was the highest in it’s pathogene process compared with the CK. The change of ROS in susceptible species often appeared one peak and 2 to 3 peaks in the resistant ones. Moreover, the higher resistance to rust, the sooner occuring of second peak,and the higher of ROS value. ROS was fluctuatedly changed throughout the infection process,and the rate of ROS fluctuation rate immune and resistance in the susceptible varieties was higher than susceptible.
2、The activity of POD, SOD and CAT had a dynamic change all the time after poplar inoculated with Melampsora larici-populina Kleb., and they were cooperative controled by each other. The activity of SOD was negatively correlated with the poplar resistance. The POD activity did not change significantly in early period after inoculation, but it had negative correlation with disease resistance later. The CAT activity was highly increased in 0.5 d ,then decreased in 1 d,moreover appeared one peak in 3 d to 5 d.The higher resistance to rust the lower CAT activity.
3、The PAL activity increased rapidly and had stronger strength in the host of immune and resistance species after inoculated with Melampsora larici-populina Kleb. There were significant differences in the ration of PAL activity in each combination to the corresponding controls. The chitinase activity was positively correlated with poplar resistance basically. There were 2~3 times of peaks in the resistant poplar varieties. In the ratio with the corresponding controlls, there was significantly difference between immune and others species, but little differences in others.
4、In the pathogene process between poplar and Melampsora larici-populina Kleb.,there was very little accumulation of lignin in 1 d to 2 d in the leave tissue of incompatible combinations and comparatively obvious accumulation in 3 d. But lignin almost had no accumulation in the compatible one and healthy control, while more accumulation in highly resistant poplar varieties. There was no correlation between the accumucation of lignin and poplar rust resistance.
5、Using DAPI stain after slicing the poplar leaves ,there was a strong blue light in mucli under the fluorescence microscope. The nucleolus were round or nearly round in the healthy leaves of different poplar varieties. There was HR phenomena and significantly change of PCD in P. szechuanica after inoculated with Melampsora larici-populina Kleb. The nuclei began to change in 0.5d after inoculation, then cracked in 5 d, disappeared in 7 d at last. However we found HR phenomenon after the inoculation of Populus purdomii,but it did not belong to PCD process.
引文
白志英,王冬梅. 2003.小麦与叶锈菌互作过程中细胞程序性死亡的细胞学观察.实验生物学报.36 (5): 357～360
曹支敏,李振岐,胡锦江. 1998.落叶松-杨栅锈菌(Melampsora larici-populina Kleb.)生理分化研究.西北林学院学报,13(1): 53～57
曹支敏,余仲东,潘彦平,任本权. 2005.中国落叶松-杨栅锈菌(Melam psorala rici-populina Kleb.)生理小种分化.植物病理学报,35(2): 184～186
曾永三,王振中. 1999.苯丙氨酸解氨酶在植物抗病反应中的作用.仲恺农业技术学院学报,12 3): 56～65
曾永三,王振中. 2003.苯丙氨酸解氨酶和过氧化氢酶活性与豇豆抗锈病性的关系.仲恺农业技术学院学报,16 (1): 1～5
蔡新忠,宋凤鸣,郑重.1995.植物病程相关蛋白.植物生理学通讯,31(2):129~ 136
曾永三,王振中. 2004.豇豆与锈菌互作中的活性氧代谢研究.植物病理学报,34 ( 2):146～153
曾永三,王振中2003.豇豆锈菌诱导的2种酶活性与抗病性的关系.华中农业大学学报, 22(2): 117～122
陈建珍,曹支敏,樊军锋. 2005.杨树叶锈病寄主抗性调查.西北林学院学报,20 (1) : 153～155
陈利锋. 1997.抗感赤霉病小麦品种超氧化物歧化酶和过氧化物酶的活性比较.植物病理学报,27(3):309-312
陈玉惠,叶建仁,魏初奖. 2002.松材线虫对黑松、湿地松幼苗活性氧代谢的影响.南京林业大学学报:自然科学版,26(4):19～22
戴芳澜. 1979.中国真菌总汇,北京:科学出版社:386-396
刁毅. 2006.植物诱导抗病性的结构抗性机制.攀枝花学院学报,23 (1): 116～118
董海丽,井金学. 2003.活性氧和一氧化氮在植物抗病反应中的作用.西北农林科技大学学报(自然科学版),31 (1): 161～164
杜林,曹支敏.2010.落叶松-杨栅锈菌立体培养方法研究.林业实用技术,2:30～34
杜秀敏,殷文璇,赵彦修,张慧. 2001.植物中活性氧的产生及清除机制.生物工程学报,17 (2): 121～125
樊自红. 1989.过氧化物酶和苯丙氨酸解氨酶与毛白杨抗锈性的关系.植物病理学报,19(2):95～100
高爱琴,余仲东,王建国. 2004.美洲黑杨无性系对杨叶锈病的抗性研究.西北林学院学报2004,19(4):100～102
高俊凤. 2006.植物生理学实验指导.北京:高等教育出版社:北京:211～222
高雪. 2009.植物苯丙氨酸解氨酶研究进展.园艺博览,(1):30～33
郭文硕. 2002.杉木对炭疽病的抗性与苯丙氨酸解氨酶的关系.应用与环境生物学报,8(6): 592～595
韩建东,曹远银. 2009. POD和PAL在小麦抗秆锈病中的动态变化.江苏农业科学,2:109～110
胡景江,曹支敏,文建雷. 2000.落叶松-杨栅锈菌寄主抗病性的研究.林业科学研究,,13(专):114-118.
胡景江,朱玮,文建雷.1999.杨树细胞壁HRGP和木质素的诱导积累与其对溃疡病抗性的关系.植物病理学报.20(2)
黄娅琳.2009.植物中程序性细胞死亡研究进展。安徽农业科学,37 (29):14016—14018
贾显禄. 1997.小麦与小麦杆锈菌互作及非亲和机制研究.沈阳:沈阳农业大学(没有页码,但是如果是学位论文的话,可以不需要页码,但是得表明是硕士还是博士论文)
吕波,刘俊,徐朗莱.2000.小麦叶片中H2O2的3种测定方法比较.南京农业大学学报.,23 (2):101～104
江昌俊,余有本. 2001.苯丙氨酸解氨酶的研究进展.安徽农业大学学报, 28(4): 425～430
蒋选利,李振岐,康振生. 2002.小麦与条锈菌互作中过氧化酶的细胞化学研究.西北植物学报,22(3):516～520
金广峰,杨彦玲. 2006.不同杨树品种对青杨锈病抗病性调查与分析.河北林业科技,3:19
蓝海燕,陈正华. 1996.植物与病原真菌互作的形态变化及其生理、生化机制和基因调控.植物学通报1999 ,16 (4) :345～351
李堆淑. 2008.植物诱导抗病性机制的研究进展.商洛学院学报,22 (2): 46～50
李红玉,吴健胜,宋从风. 1999.水稻IR26悬浮细胞与白叶枯病菌互作的过敏反应现象.植物病理学报,29(4): 299～303
李兰真,赵会杰,杨会武.1999.小麦锈病与活性氧代谢的关系.植物生理通讯,35(2):115～117
李征,刘登义,王育鹏,丁佳红,王广林. 2006.活性氧在植物—病原物相互作用过程中的作用.安徽师范大学学报(自然科学版), 29 (1): 70～74
李忠光,龚明.2005.植物中超氧阴离子自由基测定方法的改进.云南植物研究,27 (2):211～216
梁英梅,田呈明,康振生,李振岐. 2001.青杨叶锈病菌在落叶松上发育过程的电子显微镜观察.西北林学院学报2001,16(2):31～34
刘爱新,李多川,王金生,董汉松.2005.Harpinx00诱导烟草过敏性细胞死亡的细胞集分子特征.中国农业科学,38(12):2446~2450
刘春梅,曹支敏,余仲东. 2008.中国落叶松-杨栅锈菌生理小种鉴定.西北林学院学报2008, 23(2): 105～108
刘慧英,朱祝军,吕国华.2004.低温胁迫对嫁接西瓜耐冷性和活性氧清除系统的影响.应用生态学,15(4):659-662
刘俊,吕波,徐朗莱. 2000.植物叶片中过氧化氢含量测定方法的改进,27(5)548~551
刘莉丽,曹支敏,樊军锋,王云果,余仲东,费昭雪. 2008.杨树品种叶锈病抗病性研究.西北林学院学报,3( 6): 132～134
刘美青,李淑玲. 1998.杨树抗性研究的现状及展望.河南农业大学学报,32 ( 3):253～257
刘守伟,吴凤芝,马艳玲. 2009.枯萎病菌对不同抗性黄瓜品种几种酶活性的影响.植物保护,5 (1):82～85
刘亚光,徐刚,杨庆凯. 2003.大豆叶片内几丁质酶活性的变化与大豆抗灰斑病关系的研究,东北农业大学学报,32 (2):210～218
芦光新,胡东维,徐颖. 2006.活性氧积累与小麦抗白粉病关系的研究.麦类作物学报,6 (4):149～153
陆万香. 2001.根癌农杆菌介导几丁质酶基因和β- 1, 3 -葡聚糖酶基因转入甘蓝型油菜.西南农业大学学报,3(5): 3～15
孟繁荣,李国臣,石春玲等. 1996.抗青杨叶锈病杨树品种序列的筛选.林业科技,21 (2):39～40.
孟亮,崔德才. 2004.植物几丁质酶及其在抗真菌病害中的应用.生物技术通讯,15 (4):420～422
潘彦平. 2002.落叶松-杨栅锈菌(Melampsora larici-populina Kleb.)生理小种分化及其寄主抗病性研究. [硕士学位论文].杨凌:西北农林科技大学:
祁艳,刘刚,候春燕,王冬梅.2008.小麦与叶锈菌互作过程中的H2O2与HR,分子生物学报,41 (4):245~254
任本权,曹支敏,潘彦平,余仲东. 2003.落叶松-杨栅锈菌致病性分化研究[J].西北林学院学报,18(2): 51~54
史娟,胡景江,王红玲,满丽梅,张永丽. 2002.霜霉病菌对葡萄细胞壁水解酶的诱导作用与寄主抗病性的关系.西北林学院学报,17(1):42~44
苏金为,王湘平.2002.镉诱导的茶树苗膜脂过氧化合细胞程序性死亡.植物生理与分子生物学报,28 (4):292~298
覃鹏,刘飞虎,梁雪妮. 2002.超氧化物歧化酶与植物抗逆性.黑龙江农业科学1: 31～34
田呈明,曹支敏,梁英梅. 2009.中国杨树叶锈病的研究进展[A].第二届中国林业学术大会——S5森林病害及其防治论文集[C]
田呈明,康振生,曹支敏等. 2000b.用叶盘法测定杨树对落叶松-杨栅锈菌(Melampsora larici-populina Kleb.)的抗性.林业科学研究,13(专): 119～124
田呈明,康振生,李振岐,赵彦修. 2001.杨树叶锈病组织病理学和细胞学研究.西北林学院学报,6 (2):43～49
田呈明,梁英梅,康振生,李振岐,赵彦修. 2001.杨树与栅锈菌互作的组织病理学研究.林业科学, 37 (6):52～58
田呈明,梁英梅,康振生,李振岐,赵彦修. 2002a.青杨叶锈病菌(Melampsora larici-populina Kleb.)侵染过程的超微结构研究.植物病理学报,32 (1) 71～78
田呈明,梁英梅,康振生,李振岐,赵彦修. 2002b.杨树与栅锈菌互作的细胞学研究.林业科学,38 (3):87～93
田呈明,赵鹏,曹支敏. 2008.细胞壁降解酶在落叶松-杨栅锈菌与寄主互作过程中的作用.林业科学, 44 (5):79～83
万雪琴,夏新莉,尹伟伦. 2006. 31个杂交杨无性系对青杨叶锈病的抗性评价.林业科学,31 (5):22～25
王爱国,罗广华. 1990.植物的超氧物自由基与羟胺反应的定量关系.植物生理学通讯,1990(6):55～57
王宝山. 1988.生物自由基与植物膜伤害.植物生理学通讯,(2): 12～16.
王保通,商鸿生. 2003.小麦高温抗条锈性的组织病理学和超微结构变化.植物保护学报,30 (2): 119～124
王晨芳,黄丽丽,张宏昌,韩青梅,朱琳,冯浩,康振生. 2009.小麦一条锈菌互作过程中活性氧及保护酶系的变化研究.植物病理学报,39 (1):52～60
王丰,云兴福,李蕾. 2009.机械损伤对黄瓜幼苗体内苯丙氨酸解氨酶和几丁质酶活性的影响.内蒙古农业大学学报,30 (1):36～40
王凤乐,商鸿生,李振岐. 1995.中国小麦条锈菌生理小种同工酶分析.植物病理学报,25(2):101～105
王宏梅,蒋选利,白春微,左希,丁海霞. 2009.不同抗性小麦品种受白粉菌侵染前后PPO、POD活性变化.种子,28( 4:14～17
王罗霞,张盛敏,陈银华. 2009.活性氧和一氧化氮在植物-病原体互作反应中的作用.热带农业科学, 29(6):70～77
王荣,梁元存,王丹丹,刘爱新,孟庆伟.2008 Parasiticein诱导烟草细胞凋亡的形态及生化特征.中国农业科学,41(6):1661-1666
王媛,梁军,张星耀. 2008.抗、感病杨树与溃疡病菌互作中活性氧及相关酶的动态.南京林业大学学报(自然科学版),32(5)41～46
王媛,梁军,张星耀. 2008.植物抗病过程中的细胞程序性死亡.林业科学,4(2):43～149
魏相峰,汤会君. 2006.不同抗性烟草品种感染Pseudomonas syringae pv. tabaci病菌后几种酶活性测定.检验检疫科学,6(2):17～19
魏益宁. 1984.毛白杨叶片受马格栅锈菌侵染以后多酚氧化酶和过氧化物酶活性及同功酶谱带变化趋势的研究.北京林学院学报,3:76～95.
吴强,冯汉青,李红玉,万东石,贾秋珍,李敏权,粱厚果. 2006.条锈病侵染对小麦抗氰呼吸和活性氧代谢的影响.植物病理学报,6(1):49～56
肖婷,邝海菊,何香,兰晓君,艾尔肯?热合曼,古丽斯玛依?艾拜都拉. 2009.杨树叶锈病研究.生物技术,19(5):94～96
徐德利,宋平. 2008.大麦感染黄花叶病后POD、SOD活性变化规律的初步研究.南京师大学报(自然科学版),31 ( 2):101～103
徐晓晖,孙骏威,郭泽建. 2007.植物与病原菌互作中活性氧的检测方法.中国计量学院学报,18 (1):49～53
杨俊秀,高建社,周永学. 2005.白杨派几个无性系抗病性的测定与评价.西北林学院学报,20 (1): 41～42
余仲东,高爱琴,曹支敏. 2004.杨树抗锈性研究现状.西北植物学报,24 (6):1160～1164
余仲东. 2009.松杨栅锈菌夏孢子萌发的理化因素分析.第二届中国林业学术大会——S5森林病害及其防治论文集[C]
袁毅.1984.我国杨树叶锈病菌种类的研究.北京林学院学报,6(1):48~82
张建军. 1996.小麦品种对梭条斑花叶病毒病抗病特性的研究.Ⅱ抗病性与植株内多酚氧化酶活性、过氧化物酶活性及其同工酶酶谱的关系.华中农业大学学报,15(5):420～425
张俊华,崔崇士. 2003.不同抗性南瓜品种感染Phytophthoracapsici病菌后几种酶活性测定.东北农业大学学报,34 (2) : 124～128
张林青,程智慧,孟焕文,张倩慧. 2008.大蒜叶片活性氧及保护酶系对白腐病菌粗毒素胁迫的响应.西北植物学报,,28 (5):974～978
张淑珍,徐鹏飞,韩英鹏,张大勇,李文滨. 2006.大豆疫霉菌毒素处理大豆品种后几丁质酶活性的变化.作物杂志,3:17～19
张山林.1990杨树叶锈病损失量估计.甘肃林业科技,2:29~33
张树生,胡蕾,刘忠良,何美仙,方勇. 2006.植物体内抗病相关酶与植物抗病性的关系.安徽农学通报,12(13): 48～49
张伟丽,郭振飞. 2007.不同抗性品种柱花草接种炭疽菌后CAT、SOD活性及H202、胼胝质含量的变化.扬州大学学报(农业与生命科学版),28(2): 73～77
章慧慧,励建荣. 2007.超氧化物歧化酶的研究和应用现状.农产品加工学刊,8:29～31
赵鹏. 2007.落叶松-杨山锈菌与寄主互作的病理学生理学研究. [硕士学位论文].杨凌:西北农林科技大学
郑国华. 2001.炭疽病对批把叶片活性氧代谢和解剖结构的影响.福建农业大学学报,30 (2):175～179
周仲铭,袁毅. 1985.杨树叶锈病的研究概况.北京林学院学报,4(9):84-102.
周仲铭,沈瑞祥,贺正兴,雷增普.1979.毛白杨(Populus tomentosa Carr)对马格栅锈菌(Melampsora magnusiana Wagn)所致锈病抗病性的研究.北京林学院学报,1:61~67
左豫虎,芮海英,杨传平,刘惕若. 2008.几丁质酶活性与大豆抗疫霉根腐病的关系.植物保护,34(6):49～53
左豫虎,康振生,杨传平,芮海英,娄树宝,刘惕若.2009.β-1,3-葡聚糖酶和几丁质酶活性与大豆对疫霉根腐病抗性的关系.植物病理学报,39(6):600-607
Asada Y,Matsumoto I. 1972. The Nature of Lignin obtained from Downy Mildew-infected Japanese Radish Root. Journal of Phytopathology,73(3):208～214
Boller T, Gehri A, Mauch F. 1983. Chitinase in bean leaves: induction by ethylene, purification, properties, and possible function. Plant, 157: 22～31
Bradley DJ,Kjellbom P, Lamb CJ. 1992. Elicitor-induced and wound-induced oxidative cross-linking of a proline rich plant cell wall protein: a novel, rapid defense response. Cell, 70(1): 21～30.
Brission F L, Tenhaken R, Lamb C. 1994. Function of oxidative cross-linking of cell wall structural protein in plant disease resistance. Plant Cell, 6: 1703～1712.
Bunoaurio R,Torre G D,Montalbini P. 1987. Soluble superoxide dismutase in susceptible andresistant host-parasite complex of Phaseolus vulgaris and Uromyces phaseoli. Plantpathology,31: 178～184
Chiba Osamu. 1994. Study on the variation susceptibility and the nature of resistence of poplars to the leaf rust caused by Melampsora larici-populina Kleb. Bullitin of the Government forest Experiment Station,166~172
Chisholm ST, Coaker G, Day B, Staskawicz BJ. 2006. Host microbe interactions: Shaping the evolution of the plant immune response. Cell, 124: 803～814
Delledonne M, Murgia I, Ederle D, Sbicego PF, Biondani A, Polverari A, Lamb C. 2002. Reactive oxygen intermediates modulate nitric oxide signaling in the plant hypersensitive disease-resistance response. Plant Physiol Biochem, 40: 605～610
Desikan R, Reynolds A, Hancock JT, Neill SJ. 1998. Harpin and hydrogen peroxide both initiate programmed cell death but have differential effects on defence gene expression in Arabidopsis suspension cultures. Biochem J, 330: 115～120
Dixon RA. 2001. Natural products and plant disease resistance. Nature,411: 843～847
DokeN. 1983. Involvement of superoxide anion generation in hypersensitive response of potato tuber tissues to infection with an incompatible race of Phytophthora infestans. Physiol Plant Pathol, 23:345～347
Durner J, Wendehennne D, Klessig DF. 1998. Defense gene induction in tobacco by nitric oxide, cyclic GMP, and cyclic ADP-ribose. Proc Natl Acad Sci USA, 95: 10328～10333
Fink W,Haug M,Deising H. 1991. Early defence responses of cowpea (Vigna sinensis L.) induced by non-pathogenic rust fungi. Planta,(185):246～254
Gechev TS, Hille J. 2005. Hydrogen peroxide as a signal controlling plant programmed cell death. J Cell Biol, 168: 17～20
Glazebrook J. 2005. Contrasting Mechanisms of Defense Against Biotrophic and Necrotrophic Pathogens.Phytopathology, 43: 205～227
Glazener J A, Orlandi E W, Baker C J. 1996. The active oxygen response of cell suspensions to incompatible bacteria is not sufficient to cause hypersensitive cell death. Plant Physiol, 110: 759～763
Gozzo F. 2003. Systemic acquired resistance in crop protection: from nature to a chemical approach. Journal Agricultural Food Chemical, 51(16): 4487～4503
Greenberg JT, Yao N. 2004. The role and regulation of programmed cell death in plant-pathogen interactions. Cellular Microbiol, 6: 201～211
Heath MC. 2000. Hypersensitive response-related death. Plant Molecular Biology, 44(3):321～34
Heath Michele C. 1997. Signalling between Pathogenic Rust Fungi and Resistant or Susceptible Host Plants.
Lam E, Kato N, Lawton M. 2001. Programmed cell death, mitochondria and the plant hypersensitive response. Nature, 411: 848～853
Lamb C, Dixon R A. 1997. The oxidative burst in plant disease resistance. Annual Review of Plant Physiology and Plant Molecular Biology, 48: 251～275
Laurans F, Pilate G. 1999. Histological aspects of a hypersensitive response in poplar to Melampsora larici-populina. Phytopathology, 89(3):233～238.
Levine A,Tenhaken R,Dixon R,Lamb C. 1994.H2O2 from the oxidative burst orchestrates the plant hypersensi-tive disease resistance response. Cell, 79: 583～593
Li H Y,Wang J S.1999.Release of active oxygen species from phytopathogenic bacteria and their regulation.Chinese Science Bulletin, 44(1):71~75.
Lin z f,Li S S,Lin G Z. 1988.The accumulation of hydrogen perioxide in senescing leaves and choroplasts in relation to lipid peroxidation.Acta Phytophysiol.Sin,14(1):16~22
Mayera M A,Staplesb C R,Gil-ad L N. 2001.Mechanisms of survival of necrophic fungal plant in hosts expressing the hypersensitive response.Phytochemistry, 58:33~41
Mario Monizdesa. 1992. Rapid activation of phenylpropanoid metabolism in elicitor treated hybrid Poplar (Populus trichocarpa Tarr,& Gray X Populus deltoids Marsh) suspension-cultured cells. Plant Physiology,(98): 728～737
Mlodzianowski F,Wozny A,Siwecki R. 1983. Anatomy and ultrastructure of poplar leaves I.Leaf surface of four parental trees. Journal of Tree Sciences,2(1/2): 4～9
Naton B, Hahlbrock B,Schmelzer E. 1996. Correlation of rapid cell death with metabolic changes in fungus-infected cultured parsley cells. Plant Physiol, 112:433～444
Olson P.D,Varner.J.E. 1993.Hydrogen peroxide and lignification.The Plant Journal, 4:887～892
Pei M, Ruiz C, Bayon C, Hunter T, Lonsdale D. 2005. Pathogenic variation in poplar rust Melampsora larici-populina from England. European Journal of Plant Pathology,111(2):147～155
Pinon J, Frey P.Miots, Villar M. 2000. The problem of durable resistance in the case of poplar rust(Melampsora larici-populina).Durable Resistance Symposium, (36): 54～58
Pinon J,Frey P. 1997. Structue of Melampsora larici-populina populations on wild and cultivated popla-r. Eur.J.Plant Pathol, 103(2): 159～173.
Polverari A,Molesini B, Pezzotti M, Buonaurio R, Marte M, Delledonne M. 2003. Nitric oxide- mediated ranscriptional changes in Arabidopsis thaliana. Mol Plant-Microbe Interact, 16: 1094～1105
Rinaldi C, Kohler A. 2007. Transcript Profiling of Poplar Leaves upon Infection with Compatible andIncompatible Strains of the Foliar Rust Melampsora larici-populina. Plant Physiology, 144: 347～366
Rolk Y,Liu S J,Quidde T,et al. 2004.Functional analysis of H2O2 generating systems in Botrytis cinerea:the major Cu-Zn-superoxide dismutase(BCSOD1)congtributes to virulence on French bean,whereas a glucose oxidase(BCGOD1)is dispensable,Molecular Plant Pathology, 5(1):17~27
Ryszard S. 1990. Ultrastructure of Melampsora larici-populina. Rept.Tottori Mycol.Inst,28:95～108
Schouten A,Tenberge K B,Vermeer J ,et al. 2002.Functional analysis of an extracelluar catalase of Botrytis cinerea .Molecular Plant Pathology, 3(4):227~238
Sheng Zhang ,Song Lu,Xiao Xu,Helena Korpelainen ,Chunyang Li.2010. Changes in antioxidant enzyme activities and isozyme profiles in leaves of male and female Populus cathayana infected with Melampsora larici-populina. Tree Physiology. 30(1):116~128
Siwecki R,Werner A. 1980. Resistance mechanism involved in the penetration and colonization of poplar leaf tissues by Melampsora rust. Phytopathologia Mediterranea,19: 27～29
Siwecki R.1980. Resistance mechanisms in interactions between poplars and rust. Resistance to Diseases and Pests Inforest Trees1980:130～142
Tenhaken R, Levine A, Brisson L F, Dixon R A , Lamb C. 1995. Function of the oxidative burst in hypersensitive disease resistance. Proc Natl Acad Sci USA, 92(10): 4158～4163
Vance CP,Kirk TK, Sherwood RT. 1980. Lingnification as a mechanism of disease resistance.Ann Rev Phytopatho1.(18):259～288
Wu GS, Short BJ, Lawrence EB. 1995. Disease resistance conferred by expression of a gene encoding H2O2 -generation glucose oxidase in transgenic potato plants. Plant Cell , 7: 1357～1368.
Yoshikawa M ,Yamaoka N,Takeuchi Y.1993 .Elicitors:their significance an d primary mod es of action in the induction of plant defense rea ctions.Plant Ce ll Physiol, 34(8):1163~ 1173
Young S A, Gno A, Guikerna J A.1995. Rice catiohie peroxidaseaccumulates in xylem vessels during incompatible interactions with Xanthomonas oryzae pv.oryzae.Plant Physiology,107(4):1333～1341
曹支敏,李振岐,胡锦江. 1998.落叶松-杨栅锈菌(Melampsora larici-populina Kleb.)生理分化研究.西北林学院学报,13(1): 53～57
曹支敏,余仲东,潘彦平,任本权. 2005.中国落叶松-杨栅锈菌(Melam psorala rici-populina Kleb.)生理小种分化.植物病理学报,35(2): 184～186
曾永三,王振中. 1999.苯丙氨酸解氨酶在植物抗病反应中的作用.仲恺农业技术学院学报,12 3): 56～65
曾永三,王振中. 2003.苯丙氨酸解氨酶和过氧化氢酶活性与豇豆抗锈病性的关系.仲恺农业技术学院学报,16 (1): 1～5
蔡新忠,宋凤鸣,郑重.1995.植物病程相关蛋白.植物生理学通讯,31(2):129~ 136
曾永三,王振中. 2004.豇豆与锈菌互作中的活性氧代谢研究.植物病理学报,34 ( 2):146～153
曾永三,王振中2003.豇豆锈菌诱导的2种酶活性与抗病性的关系.华中农业大学学报, 22(2): 117～122
陈建珍,曹支敏,樊军锋. 2005.杨树叶锈病寄主抗性调查.西北林学院学报,20 (1) : 153～155
陈利锋. 1997.抗感赤霉病小麦品种超氧化物歧化酶和过氧化物酶的活性比较.植物病理学报,27(3):309-312
陈玉惠,叶建仁,魏初奖. 2002.松材线虫对黑松、湿地松幼苗活性氧代谢的影响.南京林业大学学报:自然科学版,26(4):19～22
戴芳澜. 1979.中国真菌总汇,北京:科学出版社:386-396
刁毅. 2006.植物诱导抗病性的结构抗性机制.攀枝花学院学报,23 (1): 116～118
董海丽,井金学. 2003.活性氧和一氧化氮在植物抗病反应中的作用.西北农林科技大学学报(自然科学版),31 (1): 161～164
杜林,曹支敏.2010.落叶松-杨栅锈菌立体培养方法研究.林业实用技术,2:30～34
杜秀敏,殷文璇,赵彦修,张慧. 2001.植物中活性氧的产生及清除机制.生物工程学报,17 (2): 121～125
樊自红. 1989.过氧化物酶和苯丙氨酸解氨酶与毛白杨抗锈性的关系.植物病理学报,19(2):95～100
高爱琴,余仲东,王建国. 2004.美洲黑杨无性系对杨叶锈病的抗性研究.西北林学院学报2004,19(4):100～102
高俊凤. 2006.植物生理学实验指导.北京:高等教育出版社:北京:211～222
高雪. 2009.植物苯丙氨酸解氨酶研究进展.园艺博览,(1):30～33
郭文硕. 2002.杉木对炭疽病的抗性与苯丙氨酸解氨酶的关系.应用与环境生物学报,8(6): 592～595
韩建东,曹远银. 2009. POD和PAL在小麦抗秆锈病中的动态变化.江苏农业科学,2:109～110
胡景江,曹支敏,文建雷. 2000.落叶松-杨栅锈菌寄主抗病性的研究.林业科学研究,,13(专):114-118.
胡景江,朱玮,文建雷.1999.杨树细胞壁HRGP和木质素的诱导积累与其对溃疡病抗性的关系.植物病理学报.20(2)
黄娅琳.2009.植物中程序性细胞死亡研究进展。安徽农业科学,37 (29):14016—14018
贾显禄. 1997.小麦与小麦杆锈菌互作及非亲和机制研究.沈阳:沈阳农业大学(没有页码,但是如果是学位论文的话,可以不需要页码,但是得表明是硕士还是博士论文)
吕波,刘俊,徐朗莱.2000.小麦叶片中H2O2的3种测定方法比较.南京农业大学学报.,23 (2):101～104
江昌俊,余有本. 2001.苯丙氨酸解氨酶的研究进展.安徽农业大学学报, 28(4): 425～430
蒋选利,李振岐,康振生. 2002.小麦与条锈菌互作中过氧化酶的细胞化学研究.西北植物学报,22(3):516～520
金广峰,杨彦玲. 2006.不同杨树品种对青杨锈病抗病性调查与分析.河北林业科技,3:19
蓝海燕,陈正华. 1996.植物与病原真菌互作的形态变化及其生理、生化机制和基因调控.植物学通报1999 ,16 (4) :345～351
李堆淑. 2008.植物诱导抗病性机制的研究进展.商洛学院学报,22 (2): 46～50
李红玉,吴健胜,宋从风. 1999.水稻IR26悬浮细胞与白叶枯病菌互作的过敏反应现象.植物病理学报,29(4): 299～303
李兰真,赵会杰,杨会武.1999.小麦锈病与活性氧代谢的关系.植物生理通讯,35(2):115～117
李征,刘登义,王育鹏,丁佳红,王广林. 2006.活性氧在植物—病原物相互作用过程中的作用.安徽师范大学学报(自然科学版), 29 (1): 70～74
李忠光,龚明.2005.植物中超氧阴离子自由基测定方法的改进.云南植物研究,27 (2):211～216
梁英梅,田呈明,康振生,李振岐. 2001.青杨叶锈病菌在落叶松上发育过程的电子显微镜观察.西北林学院学报2001,16(2):31～34
刘爱新,李多川,王金生,董汉松.2005.Harpinx00诱导烟草过敏性细胞死亡的细胞集分子特征.中国农业科学,38(12):2446~2450
刘春梅,曹支敏,余仲东. 2008.中国落叶松-杨栅锈菌生理小种鉴定.西北林学院学报2008, 23(2): 105～108
刘慧英,朱祝军,吕国华.2004.低温胁迫对嫁接西瓜耐冷性和活性氧清除系统的影响.应用生态学,15(4):659-662
刘俊,吕波,徐朗莱. 2000.植物叶片中过氧化氢含量测定方法的改进,27(5)548~551
刘莉丽,曹支敏,樊军锋,王云果,余仲东,费昭雪. 2008.杨树品种叶锈病抗病性研究.西北林学院学报,3( 6): 132～134
刘美青,李淑玲. 1998.杨树抗性研究的现状及展望.河南农业大学学报,32 ( 3):253～257
刘守伟,吴凤芝,马艳玲. 2009.枯萎病菌对不同抗性黄瓜品种几种酶活性的影响.植物保护,5 (1):82～85
刘亚光,徐刚,杨庆凯. 2003.大豆叶片内几丁质酶活性的变化与大豆抗灰斑病关系的研究,东北农业大学学报,32 (2):210～218
芦光新,胡东维,徐颖. 2006.活性氧积累与小麦抗白粉病关系的研究.麦类作物学报,6 (4):149～153
陆万香. 2001.根癌农杆菌介导几丁质酶基因和β- 1, 3 -葡聚糖酶基因转入甘蓝型油菜.西南农业大学学报,3(5): 3～15
孟繁荣,李国臣,石春玲等. 1996.抗青杨叶锈病杨树品种序列的筛选.林业科技,21 (2):39～40.
孟亮,崔德才. 2004.植物几丁质酶及其在抗真菌病害中的应用.生物技术通讯,15 (4):420～422
潘彦平. 2002.落叶松-杨栅锈菌(Melampsora larici-populina Kleb.)生理小种分化及其寄主抗病性研究. [硕士学位论文].杨凌:西北农林科技大学:
祁艳,刘刚,候春燕,王冬梅.2008.小麦与叶锈菌互作过程中的H2O2与HR,分子生物学报,41 (4):245~254
任本权,曹支敏,潘彦平,余仲东. 2003.落叶松-杨栅锈菌致病性分化研究[J].西北林学院学报,18(2): 51~54
史娟,胡景江,王红玲,满丽梅,张永丽. 2002.霜霉病菌对葡萄细胞壁水解酶的诱导作用与寄主抗病性的关系.西北林学院学报,17(1):42~44
苏金为,王湘平.2002.镉诱导的茶树苗膜脂过氧化合细胞程序性死亡.植物生理与分子生物学报,28 (4):292~298
覃鹏,刘飞虎,梁雪妮. 2002.超氧化物歧化酶与植物抗逆性.黑龙江农业科学1: 31～34
田呈明,曹支敏,梁英梅. 2009.中国杨树叶锈病的研究进展[A].第二届中国林业学术大会——S5森林病害及其防治论文集[C]
田呈明,康振生,曹支敏等. 2000b.用叶盘法测定杨树对落叶松-杨栅锈菌(Melampsora larici-populina Kleb.)的抗性.林业科学研究,13(专): 119～124
田呈明,康振生,李振岐,赵彦修. 2001.杨树叶锈病组织病理学和细胞学研究.西北林学院学报,6 (2):43～49
田呈明,梁英梅,康振生,李振岐,赵彦修. 2001.杨树与栅锈菌互作的组织病理学研究.林业科学, 37 (6):52～58
田呈明,梁英梅,康振生,李振岐,赵彦修. 2002a.青杨叶锈病菌(Melampsora larici-populina Kleb.)侵染过程的超微结构研究.植物病理学报,32 (1) 71～78
田呈明,梁英梅,康振生,李振岐,赵彦修. 2002b.杨树与栅锈菌互作的细胞学研究.林业科学,38 (3):87～93
田呈明,赵鹏,曹支敏. 2008.细胞壁降解酶在落叶松-杨栅锈菌与寄主互作过程中的作用.林业科学, 44 (5):79～83
万雪琴,夏新莉,尹伟伦. 2006. 31个杂交杨无性系对青杨叶锈病的抗性评价.林业科学,31 (5):22～25
王爱国,罗广华. 1990.植物的超氧物自由基与羟胺反应的定量关系.植物生理学通讯,1990(6):55～57
王宝山. 1988.生物自由基与植物膜伤害.植物生理学通讯,(2): 12～16.
王保通,商鸿生. 2003.小麦高温抗条锈性的组织病理学和超微结构变化.植物保护学报,30 (2): 119～124
王晨芳,黄丽丽,张宏昌,韩青梅,朱琳,冯浩,康振生. 2009.小麦一条锈菌互作过程中活性氧及保护酶系的变化研究.植物病理学报,39 (1):52～60
王丰,云兴福,李蕾. 2009.机械损伤对黄瓜幼苗体内苯丙氨酸解氨酶和几丁质酶活性的影响.内蒙古农业大学学报,30 (1):36～40
王凤乐,商鸿生,李振岐. 1995.中国小麦条锈菌生理小种同工酶分析.植物病理学报,25(2):101～105
王宏梅,蒋选利,白春微,左希,丁海霞. 2009.不同抗性小麦品种受白粉菌侵染前后PPO、POD活性变化.种子,28( 4:14～17
王罗霞,张盛敏,陈银华. 2009.活性氧和一氧化氮在植物-病原体互作反应中的作用.热带农业科学, 29(6):70～77
王荣,梁元存,王丹丹,刘爱新,孟庆伟.2008 Parasiticein诱导烟草细胞凋亡的形态及生化特征.中国农业科学,41(6):1661-1666
王媛,梁军,张星耀. 2008.抗、感病杨树与溃疡病菌互作中活性氧及相关酶的动态.南京林业大学学报(自然科学版),32(5)41～46
王媛,梁军,张星耀. 2008.植物抗病过程中的细胞程序性死亡.林业科学,4(2):43～149
魏相峰,汤会君. 2006.不同抗性烟草品种感染Pseudomonas syringae pv. tabaci病菌后几种酶活性测定.检验检疫科学,6(2):17～19
魏益宁. 1984.毛白杨叶片受马格栅锈菌侵染以后多酚氧化酶和过氧化物酶活性及同功酶谱带变化趋势的研究.北京林学院学报,3:76～95.
吴强,冯汉青,李红玉,万东石,贾秋珍,李敏权,粱厚果. 2006.条锈病侵染对小麦抗氰呼吸和活性氧代谢的影响.植物病理学报,6(1):49～56
肖婷,邝海菊,何香,兰晓君,艾尔肯?热合曼,古丽斯玛依?艾拜都拉. 2009.杨树叶锈病研究.生物技术,19(5):94～96
徐德利,宋平. 2008.大麦感染黄花叶病后POD、SOD活性变化规律的初步研究.南京师大学报(自然科学版),31 ( 2):101～103
徐晓晖,孙骏威,郭泽建. 2007.植物与病原菌互作中活性氧的检测方法.中国计量学院学报,18 (1):49～53
杨俊秀,高建社,周永学. 2005.白杨派几个无性系抗病性的测定与评价.西北林学院学报,20 (1): 41～42
余仲东,高爱琴,曹支敏. 2004.杨树抗锈性研究现状.西北植物学报,24 (6):1160～1164
余仲东. 2009.松杨栅锈菌夏孢子萌发的理化因素分析.第二届中国林业学术大会——S5森林病害及其防治论文集[C]
袁毅.1984.我国杨树叶锈病菌种类的研究.北京林学院学报,6(1):48~82
张建军. 1996.小麦品种对梭条斑花叶病毒病抗病特性的研究.Ⅱ抗病性与植株内多酚氧化酶活性、过氧化物酶活性及其同工酶酶谱的关系.华中农业大学学报,15(5):420～425
张俊华,崔崇士. 2003.不同抗性南瓜品种感染Phytophthoracapsici病菌后几种酶活性测定.东北农业大学学报,34 (2) : 124～128
张林青,程智慧,孟焕文,张倩慧. 2008.大蒜叶片活性氧及保护酶系对白腐病菌粗毒素胁迫的响应.西北植物学报,,28 (5):974～978
张淑珍,徐鹏飞,韩英鹏,张大勇,李文滨. 2006.大豆疫霉菌毒素处理大豆品种后几丁质酶活性的变化.作物杂志,3:17～19
张山林.1990杨树叶锈病损失量估计.甘肃林业科技,2:29~33
张树生,胡蕾,刘忠良,何美仙,方勇. 2006.植物体内抗病相关酶与植物抗病性的关系.安徽农学通报,12(13): 48～49
张伟丽,郭振飞. 2007.不同抗性品种柱花草接种炭疽菌后CAT、SOD活性及H202、胼胝质含量的变化.扬州大学学报(农业与生命科学版),28(2): 73～77
章慧慧,励建荣. 2007.超氧化物歧化酶的研究和应用现状.农产品加工学刊,8:29～31
赵鹏. 2007.落叶松-杨山锈菌与寄主互作的病理学生理学研究. [硕士学位论文].杨凌:西北农林科技大学
郑国华. 2001.炭疽病对批把叶片活性氧代谢和解剖结构的影响.福建农业大学学报,30 (2):175～179
周仲铭,袁毅. 1985.杨树叶锈病的研究概况.北京林学院学报,4(9):84-102.
周仲铭,沈瑞祥,贺正兴,雷增普.1979.毛白杨(Populus tomentosa Carr)对马格栅锈菌(Melampsora magnusiana Wagn)所致锈病抗病性的研究.北京林学院学报,1:61~67
左豫虎,芮海英,杨传平,刘惕若. 2008.几丁质酶活性与大豆抗疫霉根腐病的关系.植物保护,34(6):49～53
左豫虎,康振生,杨传平,芮海英,娄树宝,刘惕若.2009.β-1,3-葡聚糖酶和几丁质酶活性与大豆对疫霉根腐病抗性的关系.植物病理学报,39(6):600-607
Asada Y,Matsumoto I. 1972. The Nature of Lignin obtained from Downy Mildew-infected Japanese Radish Root. Journal of Phytopathology,73(3):208～214
Boller T, Gehri A, Mauch F. 1983. Chitinase in bean leaves: induction by ethylene, purification, properties, and possible function. Plant, 157: 22～31
Bradley DJ,Kjellbom P, Lamb CJ. 1992. Elicitor-induced and wound-induced oxidative cross-linking of a proline rich plant cell wall protein: a novel, rapid defense response. Cell, 70(1): 21～30.
Brission F L, Tenhaken R, Lamb C. 1994. Function of oxidative cross-linking of cell wall structural protein in plant disease resistance. Plant Cell, 6: 1703～1712.
Bunoaurio R,Torre G D,Montalbini P. 1987. Soluble superoxide dismutase in susceptible andresistant host-parasite complex of Phaseolus vulgaris and Uromyces phaseoli. Plantpathology,31: 178～184
Chiba Osamu. 1994. Study on the variation susceptibility and the nature of resistence of poplars to the leaf rust caused by Melampsora larici-populina Kleb. Bullitin of the Government forest Experiment Station,166~172
Chisholm ST, Coaker G, Day B, Staskawicz BJ. 2006. Host microbe interactions: Shaping the evolution of the plant immune response. Cell, 124: 803～814
Delledonne M, Murgia I, Ederle D, Sbicego PF, Biondani A, Polverari A, Lamb C. 2002. Reactive oxygen intermediates modulate nitric oxide signaling in the plant hypersensitive disease-resistance response. Plant Physiol Biochem, 40: 605～610
Desikan R, Reynolds A, Hancock JT, Neill SJ. 1998. Harpin and hydrogen peroxide both initiate programmed cell death but have differential effects on defence gene expression in Arabidopsis suspension cultures. Biochem J, 330: 115～120
Dixon RA. 2001. Natural products and plant disease resistance. Nature,411: 843～847
DokeN. 1983. Involvement of superoxide anion generation in hypersensitive response of potato tuber tissues to infection with an incompatible race of Phytophthora infestans. Physiol Plant Pathol, 23:345～347
Durner J, Wendehennne D, Klessig DF. 1998. Defense gene induction in tobacco by nitric oxide, cyclic GMP, and cyclic ADP-ribose. Proc Natl Acad Sci USA, 95: 10328～10333
Fink W,Haug M,Deising H. 1991. Early defence responses of cowpea (Vigna sinensis L.) induced by non-pathogenic rust fungi. Planta,(185):246～254
Gechev TS, Hille J. 2005. Hydrogen peroxide as a signal controlling plant programmed cell death. J Cell Biol, 168: 17～20
Glazebrook J. 2005. Contrasting Mechanisms of Defense Against Biotrophic and Necrotrophic Pathogens.Phytopathology, 43: 205～227
Glazener J A, Orlandi E W, Baker C J. 1996. The active oxygen response of cell suspensions to incompatible bacteria is not sufficient to cause hypersensitive cell death. Plant Physiol, 110: 759～763
Gozzo F. 2003. Systemic acquired resistance in crop protection: from nature to a chemical approach. Journal Agricultural Food Chemical, 51(16): 4487～4503
Greenberg JT, Yao N. 2004. The role and regulation of programmed cell death in plant-pathogen interactions. Cellular Microbiol, 6: 201～211
Heath MC. 2000. Hypersensitive response-related death. Plant Molecular Biology, 44(3):321～34
Heath Michele C. 1997. Signalling between Pathogenic Rust Fungi and Resistant or Susceptible Host Plants.
Lam E, Kato N, Lawton M. 2001. Programmed cell death, mitochondria and the plant hypersensitive response. Nature, 411: 848～853
Lamb C, Dixon R A. 1997. The oxidative burst in plant disease resistance. Annual Review of Plant Physiology and Plant Molecular Biology, 48: 251～275
Laurans F, Pilate G. 1999. Histological aspects of a hypersensitive response in poplar to Melampsora larici-populina. Phytopathology, 89(3):233～238.
Levine A,Tenhaken R,Dixon R,Lamb C. 1994.H2O2 from the oxidative burst orchestrates the plant hypersensi-tive disease resistance response. Cell, 79: 583～593
Li H Y,Wang J S.1999.Release of active oxygen species from phytopathogenic bacteria and their regulation.Chinese Science Bulletin, 44(1):71~75.
Lin z f,Li S S,Lin G Z. 1988.The accumulation of hydrogen perioxide in senescing leaves and choroplasts in relation to lipid peroxidation.Acta Phytophysiol.Sin,14(1):16~22
Mayera M A,Staplesb C R,Gil-ad L N. 2001.Mechanisms of survival of necrophic fungal plant in hosts expressing the hypersensitive response.Phytochemistry, 58:33~41
Mario Monizdesa. 1992. Rapid activation of phenylpropanoid metabolism in elicitor treated hybrid Poplar (Populus trichocarpa Tarr,& Gray X Populus deltoids Marsh) suspension-cultured cells. Plant Physiology,(98): 728～737
Mlodzianowski F,Wozny A,Siwecki R. 1983. Anatomy and ultrastructure of poplar leaves I.Leaf surface of four parental trees. Journal of Tree Sciences,2(1/2): 4～9
Naton B, Hahlbrock B,Schmelzer E. 1996. Correlation of rapid cell death with metabolic changes in fungus-infected cultured parsley cells. Plant Physiol, 112:433～444
Olson P.D,Varner.J.E. 1993.Hydrogen peroxide and lignification.The Plant Journal, 4:887～892
Pei M, Ruiz C, Bayon C, Hunter T, Lonsdale D. 2005. Pathogenic variation in poplar rust Melampsora larici-populina from England. European Journal of Plant Pathology,111(2):147～155
Pinon J, Frey P.Miots, Villar M. 2000. The problem of durable resistance in the case of poplar rust(Melampsora larici-populina).Durable Resistance Symposium, (36): 54～58
Pinon J,Frey P. 1997. Structue of Melampsora larici-populina populations on wild and cultivated popla-r. Eur.J.Plant Pathol, 103(2): 159～173.
Polverari A,Molesini B, Pezzotti M, Buonaurio R, Marte M, Delledonne M. 2003. Nitric oxide- mediated ranscriptional changes in Arabidopsis thaliana. Mol Plant-Microbe Interact, 16: 1094～1105
Rinaldi C, Kohler A. 2007. Transcript Profiling of Poplar Leaves upon Infection with Compatible andIncompatible Strains of the Foliar Rust Melampsora larici-populina. Plant Physiology, 144: 347～366
Rolk Y,Liu S J,Quidde T,et al. 2004.Functional analysis of H2O2 generating systems in Botrytis cinerea:the major Cu-Zn-superoxide dismutase(BCSOD1)congtributes to virulence on French bean,whereas a glucose oxidase(BCGOD1)is dispensable,Molecular Plant Pathology, 5(1):17~27
Ryszard S. 1990. Ultrastructure of Melampsora larici-populina. Rept.Tottori Mycol.Inst,28:95～108
Schouten A,Tenberge K B,Vermeer J ,et al. 2002.Functional analysis of an extracelluar catalase of Botrytis cinerea .Molecular Plant Pathology, 3(4):227~238
Sheng Zhang ,Song Lu,Xiao Xu,Helena Korpelainen ,Chunyang Li.2010. Changes in antioxidant enzyme activities and isozyme profiles in leaves of male and female Populus cathayana infected with Melampsora larici-populina. Tree Physiology. 30(1):116~128
Siwecki R,Werner A. 1980. Resistance mechanism involved in the penetration and colonization of poplar leaf tissues by Melampsora rust. Phytopathologia Mediterranea,19: 27～29
Siwecki R.1980. Resistance mechanisms in interactions between poplars and rust. Resistance to Diseases and Pests Inforest Trees1980:130～142
Tenhaken R, Levine A, Brisson L F, Dixon R A , Lamb C. 1995. Function of the oxidative burst in hypersensitive disease resistance. Proc Natl Acad Sci USA, 92(10): 4158～4163
Vance CP,Kirk TK, Sherwood RT. 1980. Lingnification as a mechanism of disease resistance.Ann Rev Phytopatho1.(18):259～288
Wu GS, Short BJ, Lawrence EB. 1995. Disease resistance conferred by expression of a gene encoding H2O2 -generation glucose oxidase in transgenic potato plants. Plant Cell , 7: 1357～1368.
Yoshikawa M ,Yamaoka N,Takeuchi Y.1993 .Elicitors:their significance an d primary mod es of action in the induction of plant defense rea ctions.Plant Ce ll Physiol, 34(8):1163~ 1173
Young S A, Gno A, Guikerna J A.1995. Rice catiohie peroxidaseaccumulates in xylem vessels during incompatible interactions with Xanthomonas oryzae pv.oryzae.Plant Physiology,107(4):1333～1341