scholarly journals Evolutionarily distinct Resistance proteins detect a pathogen effector through its association with different host targets

2021 ◽  
Author(s):  
Haixia Wang ◽  
Franziska Trusch ◽  
Dionne Turnbull ◽  
Carolina Aguilera‐Galvez ◽  
Susan Breen ◽  
...  
Pathogens ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 551
Author(s):  
Juan G. Morales ◽  
Astrid E. Gaviria ◽  
Elizabeth Gilchrist

Phytophthora infestans is a devastating plant pathogen in several crops such as potato (Solanum tuberosum), tomato (Solanum lycopersicum) and Andean fruits such as tree tomato (Solanum betaceum), lulo (Solanum quitoense), uchuva (Physalis peruviana) and wild species in the genus Solanum sp. Despite intense research performed around the world, P. infestans populations from Colombia, South America, are poorly understood. Of particular importance is knowledge about pathogen effector proteins, which are responsible for virulence. The present work was performed with the objective to analyze gene sequences coding for effector proteins of P. infestans from isolates collected from different hosts and geographical regions. Several genetic parameters, phylogenetic analyses and neutrality tests for non-synonymous and synonymous substitutions were calculated. Non-synonymous substitutions were identified for all genes that exhibited polymorphisms at the DNA level. Significant negative selection values were found for two genes (PITG_08994 and PITG_12737) suggesting active coevolution with the corresponding host resistance proteins. Implications for pathogen virulence mechanisms and disease management are discussed.


2001 ◽  
Vol 120 (5) ◽  
pp. A93-A93
Author(s):  
D ROST ◽  
J KONIG ◽  
G WEISS ◽  
E KLAR ◽  
W STREMMEL ◽  
...  

2021 ◽  
Vol 22 (6) ◽  
pp. 3085
Author(s):  
Hamza A. Alaswad ◽  
Amani A. Mahbub ◽  
Christine L. Le Maitre ◽  
Nicola Jordan-Mahy

Leukaemia is a malignant disease of the blood. Current treatments for leukaemia are associated with serious side-effects. Plant-derived polyphenols have been identified as potent anti-cancer agents and have been shown to work synergistically with standard chemotherapy agents in leukaemia cell lines. Polyphenols have multiple mechanisms of action and have been reported to decrease cell proliferation, arrest cell cycle and induce apoptosis via the activation of caspase (3, 8 and 9); the loss of mitochondrial membrane potential and the release of cytochrome c. Polyphenols have been shown to suppress activation of transcription factors, including NF-kB and STAT3. Furthermore, polyphenols have pro-oxidant properties, with increasing evidence that polyphenols inhibit the antioxidant activity of glutathione, causing oxidative DNA damage. Polyphenols also induce autophagy-driven cancer cell death and regulate multidrug resistance proteins, and thus may be able to reverse resistance to chemotherapy agents. This review examines the molecular mechanism of action of polyphenols and discusses their potential therapeutic targets. Here, we discuss the pharmacological properties of polyphenols, including their anti-inflammatory, antioxidant, anti-proliferative, and anti-tumour activities, and suggest that polyphenols are potent natural agents that can be useful therapeutically; and discuss why data on bioavailability, toxicity and metabolism are essential to evaluate their clinical use.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Xinhua Sun ◽  
Dmitry Lapin ◽  
Joanna M. Feehan ◽  
Sara C. Stolze ◽  
Katharina Kramer ◽  
...  

AbstractPlants utilise intracellular nucleotide-binding, leucine-rich repeat (NLR) immune receptors to detect pathogen effectors and activate local and systemic defence. NRG1 and ADR1 “helper” NLRs (RNLs) cooperate with enhanced disease susceptibility 1 (EDS1), senescence-associated gene 101 (SAG101) and phytoalexin-deficient 4 (PAD4) lipase-like proteins to mediate signalling from TIR domain NLR receptors (TNLs). The mechanism of RNL/EDS1 family protein cooperation is not understood. Here, we present genetic and molecular evidence for exclusive EDS1/SAG101/NRG1 and EDS1/PAD4/ADR1 co-functions in TNL immunity. Using immunoprecipitation and mass spectrometry, we show effector recognition-dependent interaction of NRG1 with EDS1 and SAG101, but not PAD4. An EDS1-SAG101 complex interacts with NRG1, and EDS1-PAD4 with ADR1, in an immune-activated state. NRG1 requires an intact nucleotide-binding P-loop motif, and EDS1 a functional EP domain and its partner SAG101, for induced association and immunity. Thus, two distinct modules (NRG1/EDS1/SAG101 and ADR1/EDS1/PAD4) mediate TNL receptor defence signalling.


Genetics ◽  
2003 ◽  
Vol 163 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Paola Fabrizio ◽  
Lee-Loung Liou ◽  
Vanessa N Moy ◽  
Alberto Diaspro ◽  
Joan Selverstone Valentine ◽  
...  

Abstract Signal transduction pathways inactivated during periods of starvation are implicated in the regulation of longevity in organisms ranging from yeast to mammals, but the mechanisms responsible for life-span extension are poorly understood. Chronological life-span extension in S. cerevisiae cyr1 and sch9 mutants is mediated by the stress-resistance proteins Msn2/Msn4 and Rim15. Here we show that mitochondrial superoxide dismutase (Sod2) is required for survival extension in yeast. Deletion of SOD2 abolishes life-span extension in sch9Δ mutants and decreases survival in cyr1:mTn mutants. The overexpression of Sods—mitochondrial Sod2 and cytosolic CuZnSod (Sod1)—delays the age-dependent reversible inactivation of mitochondrial aconitase, a superoxide-sensitive enzyme, and extends survival by 30%. Deletion of the RAS2 gene, which functions upstream of CYR1, also doubles the mean life span by a mechanism that requires Msn2/4 and Sod2. These findings link mutations that extend chronological life span in S. cerevisiae to superoxide dismutases and suggest that the induction of other stress-resistance genes regulated by Msn2/4 and Rim15 is required for maximum longevity extension.


2013 ◽  
Vol 13 (3) ◽  
pp. 347-357 ◽  
Author(s):  
Koji Yamaguchi ◽  
Kenta Yamada ◽  
Kazuya Ishikawa ◽  
Satomi Yoshimura ◽  
Nagao Hayashi ◽  
...  

2018 ◽  
Vol 31 (3) ◽  
pp. 386-398 ◽  
Author(s):  
Ronaldo José Durigan Dalio ◽  
Heros José Máximo ◽  
Tiago Silva Oliveira ◽  
Thamara de Medeiros Azevedo ◽  
Henrique Leme Felizatti ◽  
...  

Coevolution has shaped the molecular basis of an extensive number of defense mechanisms in plant-pathogen interactions. Phytophthora parasitica, a hemibiothrophic oomycete pathogen and the causal agent of citrus root rot and gummosis, interacts differently with Citrus sunki and Poncirus trifoliata, two commonly favored citrus rootstocks that are recognized as susceptible and resistant, respectively, to P. parasitica. The molecular core of these interactions remains elusive. Here, we provide evidence on the defense strategies employed by both susceptible and resistant citrus rootstocks, in parallel with P. parasitica deployment of effectors. Time course expression analysis (quantitative real-time polymerase chain reaction) of several defense-related genes were evaluated during i) plant disease development, ii) necrosis, and iii) pathogen effector gene expression. In C. sunki, P. parasitica deploys effectors, including elicitins, NPP1 (necrosis-inducing Phytophthora protein 1), CBEL (cellulose-binding elicitor and lectin activity), RxLR, and CRN (crinkler), and, consequently, this susceptible plant activates its main defense signaling pathways that result in the hypersensitive response and necrosis. Despite the strong plant-defense response, it fails to withstand P. parasitica invasion, confirming its hemibiothrophic lifestyle. In Poncirus trifoliata, the effectors were strongly expressed, nevertheless failing to induce any immunity manipulation and disease development, suggesting a nonhost resistance type, in which the plant relies on preformed biochemical and anatomical barriers.


2006 ◽  
Vol 159 (3) ◽  
pp. 169-179 ◽  
Author(s):  
Anne Lespine ◽  
Jacques Dupuy ◽  
Stéphane Orlowski ◽  
Tünde Nagy ◽  
Hristos Glavinas ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document