Cytokinin-induced cell death is associated with elevated expression of alternative oxidase in tobacco BY-2 cells
Jazyk angličtina Země Rakousko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
- MeSH
- adenosin analogy a deriváty farmakologie MeSH
- benzylové sloučeniny MeSH
- buněčná smrt fyziologie MeSH
- genetické inženýrství MeSH
- geneticky modifikované rostliny MeSH
- kinetin farmakologie MeSH
- kultivované buňky MeSH
- messenger RNA biosyntéza genetika MeSH
- mitochondrie účinky léků genetika metabolismus MeSH
- oxidoreduktasy biosyntéza genetika MeSH
- puriny MeSH
- reaktivní formy kyslíku metabolismus MeSH
- rostlinné proteiny biosyntéza genetika MeSH
- tabák cytologie účinky léků genetika metabolismus MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- adenosin MeSH
- benzylaminopurine MeSH Prohlížeč
- benzylové sloučeniny MeSH
- kinetin MeSH
- messenger RNA MeSH
- N(6)-benzyladenosine MeSH Prohlížeč
- oxidoreduktasy MeSH
- puriny MeSH
- reaktivní formy kyslíku MeSH
- rostlinné proteiny MeSH
N(6)-benzyladenine (BA) and N(6)-benzyladenosine ([9R]BA) induce massive production of reactive oxygen species (ROS) that is eventually followed by a loss of cell viability in tobacco BY-2 cells (Mlejnek et al. Plant Cell Environ 26:1723-1735, 2003, Plant Sci 168:389-395, 2005). Results presented in this work suggest that the main sources of ROS are likely mitochondria and that the maintenance of the mitochondrial transmembrane potential is crucial for ROS production in cytokinin-treaded BY-2 cells. Therefore, the possible involvement of alternative oxidase (AOX) in cell death process induced by BA and [9R]BA was studied. About three- to fourfold increase in mRNA levels of AOX1 was observed a few hours after the BA and [9R]BA addition into the growth medium. The elevated expression of AOX1 mRNA could be prevented by adding adenine and adenosine which simultaneously reduced the cytotoxic effects of BA and [9R]BA, respectively. N(6)-benzyladenine 7-β-D-glucoside ([7G]BA) which is a common non-toxic metabolite of BA and [9R]BA did not affect the AOX1 mRNA expression. Although AOX1 seemed to be involved in protection of BY-2 cells against the abiotic stress induced by BA and [9R]BA, the results do not support the idea that it protects cells from death exclusively by scavenging of reactive oxygen species. Indeed, N-propyl gallate, an inhibitor of AOX, decreased cell survival despite it concomitantly decreased the ROS production. This finding is in contrast to the effect of salicylhydroxamic acid, another well-known inhibitor of AOX, which also increased the number of dying cells while it increased the ROS production.
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