NLR functions in plant and animal immune systems: so far and yet so close

被引:347
作者
Maekawa, Takaki [1 ]
Kufer, Thomas A. [2 ]
Schulze-Lefert, Paul [1 ]
机构
[1] Max Planck Inst Plant Breeding Res, Dept Plant Microbe Interact, Cologne, Germany
[2] Univ Cologne, Inst Med Microbiol Immunol & Hyg, Cologne, Germany
关键词
ARABIDOPSIS RESISTANCE PROTEIN; RICH REPEAT PROTEIN; NB-LRR PROTEIN; DISEASE-RESISTANCE; CELL-DEATH; MILDEW RESISTANCE; CRYSTAL-STRUCTURE; STRUCTURAL BASIS; TIR DOMAIN; HYPERSENSITIVE RESPONSE;
D O I
10.1038/ni.2083
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In plants and animals, the NLR family of receptors perceives non-self and modified-self molecules inside host cells and mediates innate immune responses to microbial pathogens. Despite their similar biological functions and protein architecture, animal NLRs are normally activated by conserved microbe-or damage-associated molecular patterns, whereas plant NLRs typically detect strain-specific pathogen effectors. Plant NLRs recognize either the effector structure or effector-mediated modifications of host proteins. The latter indirect mechanism for the perception of non-self, as well as the within-species diversification of plant NLRs, maximize the capacity to recognize non-self through the use of a finite number of innate immunoreceptors. We discuss recent insights into NLR activation, signal initiation through the homotypic association of N-terminal domains and subcellular receptor dynamics in plants and compare those with NLR functions in animals.
引用
收藏
页码:818 / 826
页数:9
相关论文
共 144 条
[101]   Constitutively active Pto induces a Prf-dependent hypersensitive response in the absence of avrPto [J].
Rathjen, JP ;
Chang, JH ;
Staskawicz, BJ ;
Michelmore, RW .
EMBO JOURNAL, 1999, 18 (12) :3232-3240
[102]   Co-evolutionary interactions between host resistance and pathogen effector genes in flax rust disease [J].
Ravensdale, Michael ;
Nemri, Adnane ;
Thrall, Peter H. ;
Ellis, Jeffrey G. ;
Dodds, Peter N. .
MOLECULAR PLANT PATHOLOGY, 2011, 12 (01) :93-102
[103]   Differential recognition of highly divergent downy mildew avirulence gene alleles by RPP1 resistance genes from two Arabidopsis lines [J].
Rehmany, AP ;
Gordon, A ;
Rose, LE ;
Allen, RL ;
Armstrong, MR ;
Whisson, SC ;
Kamoun, S ;
Tyler, BM ;
Birch, PRJ ;
Beynon, JL .
PLANT CELL, 2005, 17 (06) :1839-1850
[104]   Structure of the apoptotic protease-activating factor 1 bound to ADP [J].
Riedl, SJ ;
Li, WY ;
Chao, Y ;
Schwarzenbacher, R ;
Shi, YG .
NATURE, 2005, 434 (7035) :926-933
[105]   Different roles of Enhanced Disease Susceptibility1 (EDS1) bound to and dissociated from Phytoalexin Deficient4 (PAD4) in Arabidopsis immunity [J].
Rietz, Steffen ;
Stamm, Anika ;
Malonek, Stefan ;
Wagner, Stephan ;
Becker, Dieter ;
Medina-Escobar, Nieves ;
Vlot, A. Corina ;
Feys, Bart J. ;
Niefind, Karsten ;
Parker, Jane E. .
NEW PHYTOLOGIST, 2011, 191 (01) :107-119
[106]   The maintenance of extreme amino acid diversity at the disease resistance gene, RPP13, in Arabidopsis thaliana [J].
Rose, LE ;
Bittner-Eddy, PD ;
Langley, CH ;
Holub, EB ;
Michelmore, RW ;
Beynon, JL .
GENETICS, 2004, 166 (03) :1517-1527
[107]   NOD-like receptors and human diseases [J].
Rosenstiel, Philip ;
Till, Andreas ;
Schreiber, Stefan .
MICROBES AND INFECTION, 2007, 9 (05) :648-657
[108]   New insights into innate immunity in Arabidopsis [J].
Ryan, Clarence A. ;
Huffaker, Alisa ;
Yamaguchi, Yube .
CELLULAR MICROBIOLOGY, 2007, 9 (08) :1902-1908
[109]   Pathogenicity Determinants in Smut Fungi Revealed by Genome Comparison [J].
Schirawski, Jan ;
Mannhaupt, Gertrud ;
Muench, Karin ;
Brefort, Thomas ;
Schipper, Kerstin ;
Doehlemann, Gunther ;
Di Stasio, Maurizio ;
Roessel, Nicole ;
Mendoza-Mendoza, Artemio ;
Pester, Doris ;
Mueller, Olaf ;
Winterberg, Britta ;
Meyer, Elmar ;
Ghareeb, Hassan ;
Wollenberg, Theresa ;
Muensterkoetter, Martin ;
Wong, Philip ;
Walter, Mathias ;
Stukenbrock, Eva ;
Gueldener, Ulrich ;
Kahmann, Regine .
SCIENCE, 2010, 330 (6010) :1546-1548
[110]   The Inflammasomes [J].
Schroder, Kate ;
Tschopp, Jurg .
CELL, 2010, 140 (06) :821-832