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Delay of M‐phase onset by aphidicolin can retain the nuclear localization of zinc and metallothionein in 3T3‐L1 fibroblasts
Author(s) -
Apostolova Margarita D.,
Cherian M. George
Publication year - 2000
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(200005)183:2<247::aid-jcp11>3.0.co;2-x
Subject(s) - aphidicolin , metallothionein , zinc , 3t3 cells , phase (matter) , microbiology and biotechnology , chemistry , biology , cell culture , biochemistry , cell , genetics , cell cycle , transfection , organic chemistry
The transient nuclear localization of metallothionein during cell growth and differentiation may be related to the increased requirement of zinc for DNA synthesis, activation of metalloenzymes, and transcription factors. Treatment of 3T3‐L1 fibroblasts with aphidicolin, an inhibitor of nuclear DNA synthesis, caused a cell‐cycle block at G1/S phase and a delay in the onset of M phase. This also resulted in the accumulation of both zinc and metallothionein in the nucleus. After removal of aphidicolin, the cells rapidly reentered S phase, and during the G2/M phase of cell cycle both zinc and metallothionein began to relocate to the cytoplasm. Delaying the onset of M phase in 3T3‐L1 cells could prevent the cytoplasmic relocation of metallothionein. The nuclear translocation of both zinc and metallothionein during the cell cycle can be considered as a normal process and this may be a general mechanism in response to mitogenic signals. J. Cell. Physiol. 183:247–253, 2000. © 2000 Wiley‐Liss, Inc.