Claviceps purpurea expressing polygalacturonases escaping PGIP inhibition fully infects PvPGIP2 wheat transgenic plants but its infection is delayed in wheat transgenic plants with increased level of pectin methyl esterification.

Claviceps purpurea expressing polygalacturonases escaping PGIP inhibition fully infects PvPGIP2 wheat transgenic plants but its infection is delayed in wheat transgenic plants with increased level of pectin methyl esterification.
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表达逃脱 PGIP 抑制的多聚半乳糖醛酸酶的麦角菌完全感染 PvPGIP2 小麦转基因植物,但其感染在果胶甲酯化水平增加的小麦转基因植物中被延迟。

DOI:
10.1016/j.plaphy.2013.10.011
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发表时间:
2013
期刊:
PPB
影响因子:
--
通讯作者:
Volpi C
Volpi C
中科院分区:
--
文献类型:
--
作者:
Volpi C

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麦角菌属麦角紫斑病菌侵染黑麦花的过程伴随着果胶的降解,多聚半乳糖醛酸酶(PG)活性代表了致病因子。小麦也被麦角菌感染,我们测试了多聚半乳糖醛酸酶抑制蛋白(PGIP)的存在是否会影响病原菌的感染和麦角病的发展。表达菜豆PvPGIP 2的小麦转基因植物在感染C. purpurea时没有表现出明显的疾病症状减轻。为了确定PvPGIP 2植物缺乏提高抗性的可能原因,我们在毕赤酵母中表达了存在于紫色念珠菌基因组中的两种多聚半乳糖醛酸酶cppg 1和cppg 2。为了进一步研究PG在紫茎泽兰/小麦系统中的作用,我们证明了在高度甲基酯化的果胶上,紫茎泽兰的两种PG的活性都降低。最后,我们表明,PG活性的这种降低是相关的植物,通过与过表达果胶甲基酯酶抑制剂(PMEI)的转基因小麦植株的杂交,并显示出高度的果胶甲酯化。我们观察到与无效对照相比,转基因品系中的疾病症状减少。总之,这些结果突出了果胶降解对小麦麦角病发展的重要性,并支持抑制果胶降解可能代表控制谷物中麦角的可能途径的观点。
Claviceps purpurea is a biotrophic fungal pathogen of grasses causing the ergot disease. The infection process ofC. purpureaon rye flowers is accompanied by pectin degradation and polygalacturonase (PG) activity represents a pathogenicity factor. Wheat is also infected byC. purpureaand we tested whether the presence of polygalacturonase inhibiting protein (PGIP) can affect pathogen infection and ergot disease development. Wheat transgenic plants expressing the bean PvPGIP2 did not show a clear reduction of disease symptoms when infected withC. purpurea. To ascertain the possible cause underlying this lack of improved resistance of PvPGIP2 plants, we expressed both polygalacturonases present in theC. purpureagenome,cppg1andcppg2in Pichia pastoris.In vitroassays using the heterologous expressed PGs and PvPGIP2 showed that neither PG is inhibited by this inhibitor. To further investigate the role of PG in theC. purpurea/wheat system, we demonstrated that the activity of both PGs ofC. purpureais reduced on highly methyl esterified pectin. Finally, we showed that this reduction in PG activity is relevantinplanta, by inoculating withC. purpureatransgenic wheat plants overexpressing a pectin methyl esterase inhibitor (PMEI) and showing a high degree of pectin methyl esterification. We observed reduced disease symptoms in the transgenic line compared with null controls. Together, these results highlight the importance of pectin degradation for ergot disease development in wheat and sustain the notion that inhibition of pectin degradation may represent a possible route to control of ergot in cereals.
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DOI: --
发表时间: 2008
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