Heterologous overexpression of StERF3 triggers cell death in Nicotiana benthamiana

Plant Science ◽  
2021 ◽  
pp. 111149
Author(s):  
Yetong Qi ◽  
Zhu Yang ◽  
Xinyuan Sun ◽  
Huan He ◽  
Lei Guo ◽  
...  
2012 ◽  
Vol 34 (2) ◽  
pp. 185-191 ◽  
Author(s):  
Yong Won Kang ◽  
Young Jeon ◽  
Hyun-Sook Pai

PLoS ONE ◽  
2018 ◽  
Vol 13 (4) ◽  
pp. e0195917
Author(s):  
Jin Won Lee ◽  
Woon Heo ◽  
Jinu Lee ◽  
Narae Jin ◽  
Sei Mee Yoon ◽  
...  

2012 ◽  
Vol 25 (5) ◽  
pp. 625-636 ◽  
Author(s):  
Kae Yoshino ◽  
Hiroki Irieda ◽  
Fumie Sugimoto ◽  
Hirofumi Yoshioka ◽  
Tetsuro Okuno ◽  
...  

Colletotrichum orbiculare, the causal agent of cucumber anthracnose, infects Nicotiana benthamiana. Functional screening of C. orbiculare cDNAs in a virus vector-based plant expression system identified a novel secreted protein gene, NIS1, whose product induces cell death in N. benthamiana. Putative homologues of NIS1 are present in selected members of fungi belonging to class Sordariomycetes, Dothideomycetes, or Orbiliomycetes. Green fluorescent protein–based expression studies suggested that NIS1 is preferentially expressed in biotrophic invasive hyphae. NIS1 lacking signal peptide did not induce NIS1-triggered cell death (NCD), suggesting apoplastic recognition of NIS1. NCD was prevented by virus-induced gene silencing of SGT1 and HSP90, indicating the dependency of NCD on SGT1 and HSP90. Deletion of NIS1 had little effect on the virulence of C. orbiculare against N. benthamiana, suggesting possible suppression of NCD by C. orbiculare at the postinvasive stage. The CgDN3 gene of C. gloeosporioides was previously identified as a secreted protein gene involved in suppression of hypersensitive-like response in Stylosanthes guianensis. Notably, we found that NCD was suppressed by the expression of a CgDN3 homologue of C. orbiculare. Our findings indicate that C. orbiculare expresses NIS1 at the postinvasive stage and suggest that NCD could be repressed via other effectors, including the CgDN3 homologue.


2006 ◽  
Vol 63 (2) ◽  
pp. 273-287 ◽  
Author(s):  
Wolfgang Moeder ◽  
Olga del Pozo ◽  
Duroy A. Navarre ◽  
Gregory B. Martin ◽  
Daniel F. Klessig

2021 ◽  
Author(s):  
Jennifer Prautsch ◽  
Jessica L. Erickson ◽  
Sedef Özyürek ◽  
Rahel Gormannns ◽  
Lars Franke ◽  
...  

In Nicotiana benthamiana, expression of the Xanthomonas effector XopQ triggers ROQ1-dependent ETI responses and in parallel accumulation of plastids around the nucleus and the formation of stromules. Both processes were proposed to contribute to ETI-related hypersensitive cell death and thereby to plant immunity. Whether these reactions are directly connected to ETI signaling events has not been tested. Here we utilized transient expression experiments to determine whether XopQ-mediated plastid reactions are a result of XopQ perception by ROQ1 or a consequence of XopQ virulence activity. We find that N. benthamiana mutants lacking ROQ1, both RNLs (NRG1 and ADR1) or EDS1, fail to elicit XopQ-dependent host cell death and stromule formation. Mutants lacking only NRG1 lost XopQ-dependent cell death but retained some stromule induction that was abolished in the RNL double mutant. This analysis aligns XopQ-induced stromules with the ETI signaling cascade but not to host programmed cell death. Furthermore, data reveal that XopQ-triggered plastid clustering is not strictly linked to stromule formation during ETI. Our data suggest that stromule formation, in contrast to chloroplast peri-nuclear dynamics, is an integral part of the N. benthamiana ETI response and that both RNL sub-types play a role in this ETI response.


2015 ◽  
Author(s):  
Chih-Hang Wu ◽  
Khaoula Belhaj ◽  
Tolga O. Bozkurt ◽  
Sophien Kamoun

Intracellular immune receptors of the nucleotide-binding leucine-rich repeat (NB-LRR or NLR) proteins often function in pairs, with "helper" proteins required for the activity of "sensors" that mediate pathogen recognition. The NLR helper NRC1 (NB-LRR protein required for HR-associated cell death 1) has been described as a signalling hub required for the cell death mediated by both cell surface and intracellular immune receptors in the model plant Nicotiana benthamiana. However, this work predates the availability of the N. benthamiana genome and whether NRC1 is indeed required for the reported phenotypes has not been confirmed. Here, we investigated the NRC family of solanaceous plants using a combination of genome annotation, phylogenetics, gene silencing and genetic complementation experiments. We discovered that a paralog of NRC1, we termed NRC3, is required for the hypersensitive cell death triggered by the disease resistance protein Pto but not Rx and Mi-1.2. NRC3 may also contribute to the hypersensitive cell death triggered by the receptor-like protein Cf-4. Our results highlight the importance of applying genetic complementation to validate gene function in RNA silencing experiments.


PLoS ONE ◽  
2018 ◽  
Vol 13 (1) ◽  
pp. e0191075 ◽  
Author(s):  
Jin Won Lee ◽  
Woon Heo ◽  
Jinu Lee ◽  
Narae Jin ◽  
Sei Mee Yoon ◽  
...  

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