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DNA topoisomerase II ‐dependent control of the cell cycle progression in root meristems of Allium cepa
Author(s) -
Żabka Aneta,
Polit Justyna Teresa,
Bernasińska Joanna,
Maszewski Janusz
Publication year - 2014
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10211
Subject(s) - mitosis , topoisomerase , biology , microbiology and biotechnology , cell cycle , chromatin , dna replication , meristem , dna , biochemistry , cell , gene
The catalytic ability of DNA topoisomerases (Topo) to generate short‐term DNA breaks allow these enzymes to play crucial functions in managing DNA topology during S‐phase replication, transcription, and chromatin‐remodelling processes required to achieve commitment for the onset and transition through mitosis. Our experiments on root meristem cells of onion ( Allium cepa ) were designed to gain insight into the contribution of Topo II to plant‐specific progression throughout interphase and mitosis. Irrespective of the position of the cell in interphase, the immunofluorescence of Topo II revealed similar nuclear labelling pattern with well defined signals dispersed in the nucleoplasm and the cortical zone of the nucleolus. Only weak labelling was detected in metaphase and anaphase chromosomes. Experiments with two potent anti‐Topo II agents, doxorubicin (DOX, an anthracycline) and a bisdioxopiperazine derivative, ICRF‐193, suggest that the inhibition‐mediated increase in Topo II immunofluorescence may represent a compensatory mechanism, by which an up‐regulated expression of the enzyme tends to counteract the drug‐induced loss of indispensable catalytic and relaxation functions. γ‐H2AX immunolabelling seems to indicate that both DOX‐ and ICRF‐193‐induced alterations in cell cycle progression reflect primarily the activity of the G2/M DNA damage checkpoint. Our findings provide evidence for the plant‐specific cell cycle control mechanism induced by Topo II inhibitors under DNA stress conditions.