scholarly journals A family of pathogen-induced cysteine-rich transmembrane proteins is involved in plant disease resistance

Planta ◽  
2021 ◽  
Vol 253 (5) ◽  
Author(s):  
Marciel Pereira Mendes ◽  
Richard Hickman ◽  
Marcel C. Van Verk ◽  
Nicole M. Nieuwendijk ◽  
Anja Reinstädler ◽  
...  

Abstract Main conclusion Overexpression of pathogen-induced cysteine-rich transmembrane proteins (PCMs) in Arabidopsis thaliana enhances resistance against biotrophic pathogens and stimulates hypocotyl growth, suggesting a potential role for PCMs in connecting both biological processes. Abstract Plants possess a sophisticated immune system to protect themselves against pathogen attack. The defense hormone salicylic acid (SA) is an important player in the plant immune gene regulatory network. Using RNA-seq time series data of Arabidopsis thaliana leaves treated with SA, we identified a largely uncharacterized SA-responsive gene family of eight members that are all activated in response to various pathogens or their immune elicitors and encode small proteins with cysteine-rich transmembrane domains. Based on their nucleotide similarity and chromosomal position, the designated Pathogen-induced Cysteine-rich transMembrane protein (PCM) genes were subdivided into three subgroups consisting of PCM1-3 (subgroup I), PCM4-6 (subgroup II), and PCM7-8 (subgroup III). Of the PCM genes, only PCM4 (also known as PCC1) has previously been implicated in plant immunity. Transient expression assays in Nicotiana benthamiana indicated that most PCM proteins localize to the plasma membrane. Ectopic overexpression of the PCMs in Arabidopsis thaliana resulted in all eight cases in enhanced resistance against the biotrophic oomycete pathogen Hyaloperonospora arabidopsidis Noco2. Additionally, overexpression of PCM subgroup I genes conferred enhanced resistance to the hemi-biotrophic bacterial pathogen Pseudomonas syringae pv. tomato DC3000. The PCM-overexpression lines were found to be also affected in the expression of genes related to light signaling and development, and accordingly, PCM-overexpressing seedlings displayed elongated hypocotyl growth. These results point to a function of PCMs in both disease resistance and photomorphogenesis, connecting both biological processes, possibly via effects on membrane structure or activity of interacting proteins at the plasma membrane.

2020 ◽  
Author(s):  
Marciel Pereira Mendes ◽  
Richard Hickman ◽  
Marcel C. Van Verk ◽  
Nicole Nieuwendijk ◽  
Anja Reinstädler ◽  
...  

ABSTRACTPlants possess a sophisticated immune system to protect themselves against pathogen attack. The defense hormone salicylic acid (SA) is an important player in the plant immune gene regulatory network. Using RNA-seq time series data of Arabidopsis thaliana leaves treated with SA, we identified a largely uncharacterized SA-responsive gene family of eight members that are all activated in response to various pathogens or their immune elicitors and encode small proteins with cysteine-rich transmembrane domains. Based on their nucleotide similarity and chromosomal position, the designated Pathogen-induced Cysteine-rich transMembrane protein (PCM) genes were subdivided into three subgroups consisting of PCM1-3 (subgroup I), PCM4-6 (subgroup II), and PCM7-8 (subgroup III). Of the PCM genes, only PCM4 (also known as PCC1) has previously been implicated in plant immunity. Transient expression assays in Nicotiana benthamiana indicated that most PCM proteins localize to the plasma membrane. Ectopic overexpression of the PCMs in Arabidopsis resulted in all eight cases in enhanced resistance against the biotrophic oomycete pathogen Hyaloperonospora arabidopsidis Noco2. Additionally, overexpression of PCM subgroup I genes conferred enhanced resistance to the hemi-biotrophic bacterial pathogen Pseudomonas syringae pv. tomato DC3000. Ectopic overexpression of the PCMs also affected the expression of genes related to light signaling and development, and accordingly PCM-overexpressing seedlings displayed elongated hypocotyl growth. These results point to a function of PCMs in both disease resistance and photomorphogenesis, connecting both biological processes, possibly via effects on membrane structure or activity of interacting proteins at the plasma membrane.


2012 ◽  
Vol 25 (3) ◽  
pp. 379-392 ◽  
Author(s):  
Daigo Takemoto ◽  
Maryam Rafiqi ◽  
Ursula Hurley ◽  
Greg J. Lawrence ◽  
Maud Bernoux ◽  
...  

To investigate the role of N-terminal domains of plant disease resistance proteins in membrane targeting, the N termini of a number of Arabidopsis and flax disease resistance proteins were fused to green fluorescent protein (GFP) and the fusion proteins localized in planta using confocal microscopy. The N termini of the Arabidopsis RPP1-WsB and RPS5 resistance proteins and the PBS1 protein, which is required for RPS5 resistance, targeted GFP to the plasma membrane, and mutation of predicted myristoylation and potential palmitoylation sites resulted in a shift to nucleocytosolic localization. The N-terminal domain of the membrane-attached Arabidopsis RPS2 resistance protein was targeted incompletely to the plasma membrane. In contrast, the N-terminal domains of the Arabidopsis RPP1-WsA and flax L6 and M resistance proteins, which carry predicted signal anchors, were targeted to the endomembrane system, RPP1-WsA to the endoplasmic reticulum and the Golgi apparatus, L6 to the Golgi apparatus, and M to the tonoplast. Full-length L6 was also targeted to the Golgi apparatus. Site-directed mutagenesis of six nonconserved amino acid residues in the signal anchor domains of L6 and M was used to change the localization of the L6 N-terminal fusion protein to that of M and vice versa, showing that these residues control the targeting specificity of the signal anchor. Replacement of the signal anchor domain of L6 by that of M did not affect L6 protein accumulation or resistance against flax rust expressing AvrL567 but removal of the signal anchor domain reduced L6 protein accumulation and L6 resistance, suggesting that membrane attachment is required to stabilize the L6 protein.


Genome ◽  
2000 ◽  
Vol 43 (3) ◽  
pp. 452-460 ◽  
Author(s):  
D Sillito ◽  
I AP Parkin ◽  
R Mayerhofer ◽  
D J Lydiate ◽  
A G Good

Common structural and amino acid motifs among cloned plant disease-resistance genes (R genes), have made it possible to identify putative disease-resistance sequences based on DNA sequence identity. Mapping of such R-gene homologues will identify candidate disease-resistance loci to expedite map-based cloning strategies in complex crop genomes. Arabidopsis thaliana expressed sequence tags (ESTs) with homology to cloned plant R genes (R-ESTs), were mapped in both A. thaliana and Brassica napus to identify candidate R-gene loci and investigate intergenomic collinearity. Brassica R-gene homologous sequences were also mapped in B. napus. In total, 103 R-EST loci and 36 Brassica R-gene homologous loci were positioned on the N-fo-61-9 B. napus genetic map, and 48 R-EST loci positioned on the Columbia × Landsberg A. thaliana map. The mapped loci identified collinear regions between Arabidopsis and Brassica which had been observed in previous comparative mapping studies; the detection of syntenic genomic regions indicated that there was no apparent rapid divergence of the identified genomic regions housing the R-EST loci.Key words: RFLP mapping, candidate R genes, R-gene homologues, genomic collinearity, Arabidopsis ESTs.


2015 ◽  
Vol 28 (10) ◽  
pp. 1142-1152 ◽  
Author(s):  
Vamsi J. Nalam ◽  
Syeda Alam ◽  
Jantana Keereetaweep ◽  
Barney Venables ◽  
Dehlia Burdan ◽  
...  

Fusarium graminearum causes Fusarium head blight, an important disease of wheat. F. graminearum can also cause disease in Arabidopsis thaliana. Here, we show that the Arabidopsis LOX1 and LOX5 genes, which encode 9-lipoxygenases (9-LOXs), are targeted during this interaction to facilitate infection. LOX1 and LOX5 expression were upregulated in F. graminearum–inoculated plants and loss of LOX1 or LOX5 function resulted in enhanced disease resistance in the corresponding mutant plants. The enhanced resistance to F. graminearum infection in the lox1 and lox5 mutants was accompanied by more robust induction of salicylic acid (SA) accumulation and signaling and attenuation of jasmonic acid (JA) signaling in response to infection. The lox1- and lox5-conferred resistance was diminished in plants expressing the SA-degrading salicylate hydroxylase or by the application of methyl-JA. Results presented here suggest that plant 9-LOXs are engaged during infection to control the balance between SA and JA signaling to facilitate infection. Furthermore, since silencing of TaLpx-1 encoding a 9-LOX with homology to LOX1 and LOX5, resulted in enhanced resistance against F. graminearum in wheat, we suggest that 9-LOXs have a conserved role as susceptibility factors in disease caused by this important fungus in Arabidopsis and wheat.


2018 ◽  
Author(s):  
Wangsheng Zhu ◽  
Maricris Zaidem ◽  
Anna-Lena Van de Weyer ◽  
Rafal M. Gutaker ◽  
Eunyoung Chae ◽  
...  

AbstractPlants defend themselves against pathogens by activating an array of immune responses. Unfortunately, immunity programs may also cause unintended collateral damage to the plant itself. The quantitative disease resistance gene ACCELERATED CELL DEATH 6 (ACD6) serves as a nexus for the trade-off between growth and pathogen resistance in wild populations of Arabidopsis thaliana. An autoimmune allele, ACD6-Est, first identified in the natural accession Est-1, is found in over 10% of wild strains, even though it causes a clear fitness penalty under optimal growth conditions. There is, however, extensive variation in the strength of the autoimmune phenotype expressed by strains with an ACD6-Est allele, indicative of genetic modifiers. Quantitative genetic analysis suggests that the population genetic basis of ACD6 modulation is complex, with different strains often carrying different large-effect modifiers. One modifier is SUPPRESSOR OF NPR1-1, CONSTITUTIVE 1 (SNC1), located in a highly polymorphic cluster of nucleotide-binding domain and leucine-rich repeat (NLR) immune receptor genes, which are prototypes for qualitative disease resistance genes. Allelic variation at SNC1 correlates with ACD6-Est activity in multiple accessions, and a common structural variant affecting the NL linker sequence can explain differences in SNC1 activity. Taken together, we find that an NLR gene can mask the activity of an ACD6 autoimmune allele in natural A. thaliana populations, thereby linking different arms of the plant immune system.Author summaryPlants defend themselves against pathogens by activating immune responses. Unfortunately, these can cause unintended collateral damage to the plant itself. Nevertheless, some wild plants have genetic variants that confer a low threshold for the activation of immunity. While these enable a plant to respond particularly quickly to pathogen attack, such variants might be potentially dangerous. We are investigating one such variant of the immune gene ACCELERATED CELL DEATH 6 (ACD6) in the plant Arabidopsis thaliana. We discovered that there are variants at other genetic loci that can mask the effects of an overly active ACD6 gene. One of these genes, SUPPRESSOR OF NPR1-1, CONSTITUTIVE 1 (SNC1), codes for a known immune receptor. The SNC1 variant that attenuates ACD6 activity is rather common in A. thaliana populations, suggesting that new combinations of the hyperactive ACD6 variant and this antagonistic SNC1 variant will often arise by natural crosses. Similarly, because the two genes are unlinked, outcrossing will often lead to the hyperactive ACD6 variants being unmasked again. We propose that allelic diversity at SNC1 contributes to the maintenance of the hyperactive ACD6 variant in natural A. thaliana populations.


2004 ◽  
Vol 40 (2) ◽  
pp. 225-237 ◽  
Author(s):  
Peter Coppinger ◽  
Peter P. Repetti ◽  
Brad Day ◽  
Douglas Dahlbeck ◽  
Angela Mehlert ◽  
...  

Science ◽  
1994 ◽  
Vol 265 (5180) ◽  
pp. 1856-1860 ◽  
Author(s):  
A. Bent ◽  
B. Kunkel ◽  
D Dahlbeck ◽  
K. Brown ◽  
R Schmidt ◽  
...  

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