Differential effects of lesion mimic mutants in barley on disease development by facultative pathogens.
Differential effects of lesion mimic mutants in barley on disease development by facultative pathogens.
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DOI：
10.1093/jxb/erv154
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发表时间：
2015-06
影响因子：
6.9
通讯作者：
Brown JK
中科院分区：
文献类型：
--
作者：
McGrann GR;Steed A;Burt C;Nicholson P;Brown JK
调节细胞死亡的不同途径对不同的病原体有不同的影响。MLO和NEC1都能抑制细胞死亡，它们在对病原真菌的作用中相互作用。由于错误调控的细胞死亡程序，病变模拟突变体显示出自发的坏死点和褪绿的叶片。通常，这些突变体对生物营养性病原体的抵抗力增强，但对导致坏死性疾病的兼性真菌的反应研究较少。利用一组大麦坏死病(NEC)病斑模拟突变体，探讨了细胞死亡调控的改变在青枯病、枯萎病和黄斑病发生发展中的作用。与Nex9相比，Nec8突变体表现出较低的所有三种疾病的水平，后者增加了Colo-Cygni，但减少了镰刀菌病害的症状。Nec1突变体减少了由Colo-Cygni和F.culmorum引起的疾病的发展。负细胞死亡调节因子MLO的突变降低了NEC1诱导的类似表型的损伤的严重性和F.culmorum症状的发展。在含有MLO-5等位基因的情况下，NEC1引起的症状显著减少完全消失，并且症状和真菌生物量都大于野生型。这些结果表明，参与细胞死亡调控的生理途径在对不同真菌病原体的作用中相互作用。
Different pathways that regulate cell death have distinct effects on diverse pathogens. MLO and NEC1, which both suppress cell death, interact with one another in their effects on pathogenic fungi. Lesion mimic mutants display spontaneous necrotic spots and chlorotic leaves as a result of mis-regulated cell death programmes. Typically these mutants have increased resistance to biotrophic pathogens but their response to facultative fungi that cause necrotrophic diseases is less well studied. The effect of altered cell death regulation on the development of disease caused by Ramularia collo-cygni, Fusarium culmorum and Oculimacula yallundae was explored using a collection of barley necrotic (nec) lesion mimic mutants. nec8 mutants displayed lower levels of all three diseases compared to nec9 mutants, which had increased R. collo-cygni but decreased F. culmorum disease symptoms. nec1 mutants reduced disease development caused by both R. collo-cygni and F. culmorum. The severity of the nec1-induced lesion mimic phenotype and F. culmorum symptom development was reduced by mutation of the negative cell death regulator MLO. The significant reduction in R. collo-cygni symptoms caused by nec1 was completely abolished in the presence of the mlo-5 allele and both symptoms and fungal biomass were greater than in the wild-type. These results indicate that physiological pathways involved in regulation of cell death interact with one another in their effects on different fungal pathogens.
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