scholarly journals Plant-induced cell death in the oomycete pathogen Phytophthora parasitica

2005 ◽  
Vol 7 (9) ◽  
pp. 1365-1378 ◽  
Author(s):  
Eric Galiana ◽  
Marie-Pierre Rivière ◽  
Sophie Pagnotta ◽  
Emmanuel Baudouin ◽  
Franck Panabières ◽  
...  
2015 ◽  
Vol 28 (8) ◽  
pp. 913-926 ◽  
Author(s):  
Ke-Chun Peng ◽  
Chao-Wen Wang ◽  
Chih-Hang Wu ◽  
Chun-Tzu Huang ◽  
Ruey-Fen Liou

During host-pathogen interactions, pattern recognition receptors form complexes with proteins, such as receptor-like kinases, to elicit pathogen-associated molecular pattern-triggered immunity (PTI), an evolutionarily conserved plant defense program. However, little is known about the components of the receptor complex, as are the molecular events leading to PTI induced by the oomycete Phytophthora pathogen. Here, we demonstrate that tomato (Solanum lycopersicum) SlSOBIR1 and SlSOBIR1-like genes are involved in defense responses to Phytophthora parasitica. Silencing of SlSOBIR1 and SlSOBIR1-like enhanced susceptibility to P. parasitica in tomato. Callose deposition, reactive oxygen species production, and PTI marker gene expression were compromised in SlSOBIR1- and SlSOBIR1-like–silenced plants. Interestingly, P. parasitica infection and elicitin (ParA1) treatment induced the relocalization of SlSOBIR1 from the plasma membrane to endosomal compartments and silencing of NbSOBIR1 compromised ParA1-mediated cell death on Nicotiana benthamiana. Moreover, the SlSOBIR1 kinase domain is indispensable for ParA1 to trigger SlSOBIR1 internalization and plant cell death. Taken together, these results support the idea of participation of solanaceous SOBIR1/EVR homologs in the perception of elicitins and indicate their important roles in plant basal defense against oomycete pathogens.


PLoS ONE ◽  
2011 ◽  
Vol 6 (11) ◽  
pp. e28114 ◽  
Author(s):  
Meixiang Zhang ◽  
Qinhu Wang ◽  
Ke Xu ◽  
Yuling Meng ◽  
Junli Quan ◽  
...  

BMC Genomics ◽  
2014 ◽  
Vol 15 (1) ◽  
pp. 538 ◽  
Author(s):  
Agnès Attard ◽  
Edouard Evangelisti ◽  
Naïma Kebdani-Minet ◽  
Franck Panabières ◽  
Emeline Deleury ◽  
...  

2018 ◽  
Vol 20 (3) ◽  
pp. 356-371 ◽  
Author(s):  
Guiyan Huang ◽  
Zhirou Liu ◽  
Biao Gu ◽  
Hong Zhao ◽  
Jinbu Jia ◽  
...  

2015 ◽  
Vol 28 (8) ◽  
pp. 927-942 ◽  
Author(s):  
Patricia Manosalva ◽  
Murli Manohar ◽  
Karl-Heinz Kogel ◽  
Hong-Gu Kang ◽  
Daniel F. Klessig

The microrchidia (MORC) proteins, a subset of the GHKL ATPase superfamily, were recently described as components involved in transcriptional gene silencing and plant immunity in Arabidopsis. To assess the role of MORC1 during resistance to Phytophthora infestans in solanaceous species, we altered the expression of the corresponding MORC1 homologs in potato, tomato, and Nicotiana benthamiana. Basal resistance to P. infestans was compromised in StMORC1-silenced potato and enhanced in overexpressing lines, indicating that StMORC1 positively affects immunity. By contrast, silencing SlMORC1 expression in tomato or NbMORC1 expression in N. benthamiana enhanced basal resistance to this oomycete pathogen. In addition, silencing SlMORC1 further enhanced resistance conferred by two resistance genes in tomato. Transient expression of StMORC1 in N. benthamiana accelerated cell death induced by infestin1 (INF1), whereas SlMORC1 or NbMORC1 suppressed it. Domain-swapping and mutational analyses indicated that the C-terminal region dictates the species-specific effects of the solanaceous MORC1 proteins on INF1-induced cell death. This C-terminal region also was required for homodimerization and phosphorylation of recombinant StMORC1 and SlMORC1, and its transient expression induced spontaneous cell death in N. benthamiana. Thus, this C-terminal region likely plays important roles in both determining and modulating the biological activity of MORC1 proteins.


2020 ◽  
Vol 21 (4) ◽  
pp. 541-554 ◽  
Author(s):  
Qiang Zhang ◽  
Weiwei Li ◽  
Jiapeng Yang ◽  
Junjie Xu ◽  
Yuling Meng ◽  
...  

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Tingting Chen ◽  
Jing Peng ◽  
Xiao Yin ◽  
Meijie Li ◽  
Gaoqing Xiang ◽  
...  

AbstractPlant pathogenic oomycetes deliver a troop of effector proteins into the nucleus of host cells to manipulate plant cellular immunity and promote colonization. Recently, researchers have focused on identifying how effectors are transferred into the host cell nucleus, as well as the identity of the nuclear targets. In this study, we found that the RxLR effector PvAVH53 from the grapevine (Vitis vinifera) oomycete pathogen Plasmopara viticola physically interacts with grapevine nuclear import factor importin alphas (VvImpα and VvImpα4), localizes to the nucleus and triggers cell death when transiently expressed in tobacco (Nicotiana benthamiana) cells. Deletion of a nuclear localization signal (NLS) sequence from PvAVH53 or addition of a nuclear export signal (NES) sequence disrupted the nuclear localization of PvAVH53 and attenuated its ability to trigger cell death. Suppression of two tobacco importin-α genes, namely, NbImp-α1 and NbImp-α2, by virus-induced gene silencing (VIGS) also disrupted the nuclear localization and ability of PvAVH53 to induce cell death. Likewise, we transiently silenced the expression of VvImpα/α4 in grape through CRISPR/Cas13a, which has been reported to target RNA in vivo. Finally, we found that attenuating the expression of the Importin-αs genes resulted in increased susceptibility to the oomycete pathogen Phytophthora capsici in N. benthamiana and P. viticola in V. vinifera. Our results demonstrate that importin-αs are required for the nuclear localization and function of PvAVH53 and are essential for host innate immunity. The findings provide insight into the functions of importin-αs in grapevine against downy mildew.


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