title: ROS signaling in the hypersensitive response: when, where and what for?
abstract: Plants generally react to the attack of non-host and incompatible host microorganisms by inducing pathogenesis-related (PR) genes and localised cell death (LCD) at the site of infection, a process collectively known as the hypersensitive response (HR). Reactive oxygen species (ROS) are generated in various sub-cellular compartments shortly after pathogen recognition, and proposed to cue subsequent orchestration of the HR. Although apoplast-associated ROS production by plasma membrane NADPH oxidases have been most thoroughly studied, recent observations suggest that ROS are generated in chloroplasts earlier in the response and play a key role in execution of LCD. A model is presented in which the initial outcome of successful pathogen detection is ROS accumulation in plastids, likely mediated by mitogen-activated protein kinases and caused by dysfunction of the photosynthetic electron transport chain. ROS signaling is proposed to spread from plastids to the apoplast, through the activation of NADPH oxidases, and from there to adjacent cells, leading to suicidal death in the region of attempted infection.
authors.affiliation: Instituto de Biología Molecular y Celular de Rosario (IBR-CONICET), Universidad Nacional de Rosario, Rosario, Argentina.
authors.forename: Matias D
authors.initials: MD
authors.lastname: Zurbriggen
authors.forename: Néstor
authors.initials: N
authors.lastname: Carrillo
authors.forename: Mohammad-Reza
authors.initials: MR
authors.lastname: Hajirezaei
references.citation: Plant Physiol. 2005 Nov;139(3):1291-303
references.pmid: 16244149
references.citation: Proc Natl Acad Sci U S A. 2007 Jul 3;104(27):11495-500
references.pmid: 17592141
references.citation: Plant Physiol. 2005 Jul;138(3):1516-26
references.pmid: 15980200
references.citation: Mol Cells. 2009 Oct 31;28(4):321-9
references.pmid: 19830396
references.citation: Plant Cell Physiol. 2006 Nov;47(11):1509-19
references.pmid: 17012741
references.citation: Curr Opin Plant Biol. 2003 Aug;6(4):390-6
references.pmid: 12873535
references.citation: Environ Sci Technol. 2007 Jun 1;41(11):4071-6
references.pmid: 17612192
references.citation: Nat Genet. 2005 Oct;37(10):1130-4
references.pmid: 16170317
references.citation: Plant Cell. 2005 Mar;17(3):957-70
references.pmid: 15705948
references.citation: Trends Biotechnol. 2008 Oct;26(10):531-7
references.pmid: 18706721
references.citation: Trends Plant Sci. 2005 Jul;10(7):339-46
references.pmid: 15953753
references.citation: Plant Cell. 2006 Feb;18(2):397-411
references.pmid: 16387834
references.citation: Plant Signal Behav. 2008 Nov;3(11):920-2
references.pmid: 19513193
references.citation: Plant Physiol. 2006 Jun;141(2):391-6
references.pmid: 16760493
references.citation: Plant J. 2002 Feb;29(3):269-79
references.pmid: 11844105
references.citation: J Exp Bot. 2008;59(3):501-20
references.pmid: 18079135
references.citation: Plant Physiol. 2006 Aug;141(4):1482-93
references.pmid: 16798947
references.citation: Plant Cell. 2008 Sep;20(9):2339-56
references.pmid: 18790826
references.citation: IUBMB Life. 2007 Apr-May;59(4-5):355-60
references.pmid: 17505975
references.citation: Curr Opin Plant Biol. 2005 Aug;8(4):397-403
references.pmid: 15939662
references.citation: Trends Plant Sci. 2008 Nov;13(11):589-95
references.pmid: 18824399
references.citation: Curr Opin Plant Biol. 2005 Aug;8(4):378-82
references.pmid: 15922650
references.citation: Proc Natl Acad Sci U S A. 1999 Nov 23;96(24):14165-70
references.pmid: 10570216
references.citation: Plant J. 2009 Dec;60(6):962-73
references.pmid: 19719480
references.citation: Plant J. 2007 Sep;51(6):941-54
references.pmid: 17651371
references.citation: Plant Cell. 2006 Aug;18(8):2035-50
references.pmid: 16829589
references.citation: EMBO J. 2004 Aug 4;23(15):3072-82
references.pmid: 15272302