Recovery of tobacco cells from cadmium stress is accompanied by DNA repair and increased telomerase activity
Language English Country England, Great Britain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
12379781
DOI
10.1093/jxb/erf080
Knihovny.cz E-resources
- MeSH
- Apoptosis drug effects physiology MeSH
- Chromatin metabolism MeSH
- DNA, Plant genetics metabolism MeSH
- Cadmium pharmacology MeSH
- Cells, Cultured MeSH
- DNA Repair drug effects physiology MeSH
- Electrophoresis, Gel, Pulsed-Field MeSH
- Sulfates pharmacology MeSH
- Cadmium Compounds pharmacology MeSH
- Nicotiana cytology drug effects genetics MeSH
- Telomerase metabolism MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- cadmium sulfate MeSH Browser
- Chromatin MeSH
- DNA, Plant MeSH
- Cadmium MeSH
- Sulfates MeSH
- Cadmium Compounds MeSH
- Telomerase MeSH
It has been shown previously that apoptosis of tobacco cells induced by cadmium ions shows a relatively long lag period between exposure and cell death. This lag phase lasts for 3 d in TBY-2 cell cultures and is characterized by the maintenance of full cell viability despite extensive fragmentation of DNA into pieces of chromatin loop size. Experiments reported here demonstrate that cell death can be prevented if 50 micro M CdSO(4) is removed from the growth medium during the lag phase, suggesting that an irreversible apoptotic trigger is delivered within 24 h, between the third and fourth days of cadmium treatment. The post-cadmium recovery phase was characterized by DNA repair at the level of 50-200 kb and increased telomerase activity. Analysis of high-molecular-weight DNA by pulsed-field-gel electrophoresis revealed that the majority of DNA strand breaks was repaired within 48 h after cadmium withdrawal. Telomerase activity increased 2.5-fold in the recovery phase, but elevated levels were also found in cell extracts from apoptotic cells suggesting that telomerase might be associated with DNA repair, but it is not capable of inhibiting ongoing apoptosis. Limited exposure of TBY-2 cells to cadmium elicits non-random DNA damage of relatively high magnitude that can be repaired. It is proposed that plants might have developed a highly efficient DNA repair system to cope with transient genotoxic stress.
References provided by Crossref.org
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