An NB-LRR protein required for HR signalling mediated by both extra- and intracellular resistance proteins

2007 ◽  
Vol 50 (1) ◽  
pp. 14-28 ◽  
Author(s):  
Suzan H.E.J. Gabriëls ◽  
Jack H. Vossen ◽  
Sophia K. Ekengren ◽  
Gerben van Ooijen ◽  
Ahmed M. Abd-El-Haliem ◽  
...  
2008 ◽  
Vol 21 (1) ◽  
pp. 7-19 ◽  
Author(s):  
Teresa A. Sweat ◽  
Jennifer M. Lorang ◽  
Erica G. Bakker ◽  
Thomas J. Wolpert

The fungus Cochliobolus victoriae, the causal agent of Victoria blight, produces a compound called victorin that is required for pathogenicity of the fungus. Victorin alone reproduces disease symptoms on sensitive plants. Victorin sensitivity and susceptibility to C. victoriae were originally described on oats but have since been identified on Arabidopsis thaliana. Victorin sensitivity and disease susceptibility in Arabidopsis are conferred by LOV1, a coiled-coil-nucleotide-binding-leucine-rich repeat (CC-NB-LRR) protein. We sequenced the LOV1 gene from 59 victorin-insensitive mutants and found that the spectrum of mutations causing LOV1 loss of function was similar to that found to cause loss of function of RPM1, a CC-NB-LRR resistance protein. Also, many of the mutated residues in LOV1 are in conserved motifs required for resistance protein function. These data indicate that LOV1 may have a mechanism of action similar to resistance proteins. Victorin sensitivity was found to be the prevalent phenotype in a survey of 30 Arabidopsis ecotypes, and we found very little genetic variation among LOV1 alleles. As selection would not be expected to preserve a functional LOV1 gene to confer victorin sensitivity and disease susceptibility, we propose that LOV1 may function as a resistance gene to a naturally-occurring pathogen of Arabidopsis.


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

2021 ◽  
Vol 534 ◽  
pp. 206-211
Author(s):  
Jianzhong Huang ◽  
Xiaoqiu Wu ◽  
Kaiting Sun ◽  
Zhiyong Gao

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.


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.


2012 ◽  
Vol 11 (3) ◽  
pp. 253-263 ◽  
Author(s):  
Zhibin Zhang ◽  
Yaling Wu ◽  
Minghui Gao ◽  
Jie Zhang ◽  
Qing Kong ◽  
...  

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