Lipoxygenase in singlet oxygen generation as a response to wounding: in vivo imaging in Arabidopsis thaliana
Jazyk angličtina Země Anglie, Velká Británie Médium electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
28851974
PubMed Central
PMC5575249
DOI
10.1038/s41598-017-09758-1
PII: 10.1038/s41598-017-09758-1
Knihovny.cz E-zdroje
- MeSH
- Arabidopsis MeSH
- fenotyp MeSH
- fluorescenční protilátková technika MeSH
- konfokální mikroskopie MeSH
- lipoxygenasa metabolismus MeSH
- lipoxygenasy genetika MeSH
- mastné kyseliny metabolismus MeSH
- molekulární zobrazování MeSH
- mutace MeSH
- proteiny huseníčku genetika MeSH
- rány a poranění metabolismus MeSH
- singletový kyslík metabolismus MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- lipoxygenasa MeSH
- lipoxygenase 2, Arabidopsis MeSH Prohlížeč
- lipoxygenasy MeSH
- mastné kyseliny MeSH
- proteiny huseníčku MeSH
- singletový kyslík MeSH
Wounding, one of the most intensive stresses influencing plants ontogeny and lifespan, can be induced by herbivory as well as by physical factors. Reactive oxygen species play indispensable role both in the local and systemic defense reactions which enable "reprogramming" of metabolic pathways to set new boundaries and physiological equilibrium suitable for survival. In our current study, we provide experimental evidence on the formation of singlet oxygen (1O2) after wounding of Arabidopsis leaves. It is shown that 1O2 is formed by triplet-triplet energy transfer from triplet carbonyls to molecular oxygen. Using lipoxygenase inhibitor catechol, it is demonstrated that lipid peroxidation is initiated by lipoxygenase. Suppression of 1O2 formation in lox2 mutant which lacks chloroplast lipoxygenase indicates that lipoxygenase localized in chloroplast is predominantly responsible for 1O2 formation. Interestingly, 1O2 formation is solely restricted to chloroplasts localized at the wounding site. Data presented in this study might provide novel insight into wound-induced signaling in the local defense reaction.
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