Sohee Cho" /> Sohee Cho, Jihoon Park, and Eun Seong Hwang*

" /> Sohee Cho, Jihoon Park, and Eun Seong Hwang*

. Mol. Cells 2011;31:539-46. https://doi.org/10.1007/s10059-011-1032-4">
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Mol. Cells 2011; 31(6): 539-546

Published online June 30, 2011

https://doi.org/10.1007/s10059-011-1032-4

© The Korean Society for Molecular and Cellular Biology

Kinetics of the Cell Biological Changes Occurring in the Progression of DNA Damage-Induced Senescence

Sohee Cho1, Jihoon Park1,2, and Eun Seong Hwang1,*

1Department of Life Science, University of Seoul, Seoul 130-743, Korea, 2Present address: Yoo’s Pharm. Corp., Seoul 153-803, Korea

Correspondence to : *Correspondence: eshwang@uos.ac.kr

Received: February 21, 2011; Accepted: March 15, 2011

Abstract

Cellular senescence is characterized by cell-cycle arrest accompanied by various cell biological changes. Although these changes have been heavily relied on as senescence markers in numerous studies on senescence and its intervention, their underlying mechanisms and relationship to each other are poorly understood. Furthermore, the depth and the reversibility of those changes have not been addressed previously. Using flow cytometry coupled with confocal microscopy and Western blotting, we quantified various senescence-associated cellular changes and determined their time course profiles in MCF-7 cells undergoing DNA damage-induced senescence. The examined properties changed with several different kinetics patterns. Autofluorescence, side scattering, and the mitochondria content increased progressively and linearly. Cell volume, lysosome content, and reactive oxygen species (ROS) level increased abruptly at an early stage. Meanwhile, senescence associated ß-galactosidase activity increased after a lag of a few days. In addition, during the senescence progression, lysosomes exhibited a loss of integrity, which may have been associated with the accumulation of ROS. The finding that various senescence phenotypes matured at different rates with different lag times suggests multiple independent mechanisms controlling the expression of senescence phenotypes. This type of kinetics study would promote the understanding of how cells become fully senescent and facilitate the screening of methods that intervene in cellular senescence.

Keywords lipofuscin, lysosome, mitochondria, ROS, SA ß-Gal, senescence phenotype

Article

Research Article

Mol. Cells 2011; 31(6): 539-546

Published online June 30, 2011 https://doi.org/10.1007/s10059-011-1032-4

Copyright © The Korean Society for Molecular and Cellular Biology.

Kinetics of the Cell Biological Changes Occurring in the Progression of DNA Damage-Induced Senescence

Sohee Cho1, Jihoon Park1,2, and Eun Seong Hwang1,*

1Department of Life Science, University of Seoul, Seoul 130-743, Korea, 2Present address: Yoo’s Pharm. Corp., Seoul 153-803, Korea

Correspondence to:*Correspondence: eshwang@uos.ac.kr

Received: February 21, 2011; Accepted: March 15, 2011

Abstract

Cellular senescence is characterized by cell-cycle arrest accompanied by various cell biological changes. Although these changes have been heavily relied on as senescence markers in numerous studies on senescence and its intervention, their underlying mechanisms and relationship to each other are poorly understood. Furthermore, the depth and the reversibility of those changes have not been addressed previously. Using flow cytometry coupled with confocal microscopy and Western blotting, we quantified various senescence-associated cellular changes and determined their time course profiles in MCF-7 cells undergoing DNA damage-induced senescence. The examined properties changed with several different kinetics patterns. Autofluorescence, side scattering, and the mitochondria content increased progressively and linearly. Cell volume, lysosome content, and reactive oxygen species (ROS) level increased abruptly at an early stage. Meanwhile, senescence associated ß-galactosidase activity increased after a lag of a few days. In addition, during the senescence progression, lysosomes exhibited a loss of integrity, which may have been associated with the accumulation of ROS. The finding that various senescence phenotypes matured at different rates with different lag times suggests multiple independent mechanisms controlling the expression of senescence phenotypes. This type of kinetics study would promote the understanding of how cells become fully senescent and facilitate the screening of methods that intervene in cellular senescence.

Keywords: lipofuscin, lysosome, mitochondria, ROS, SA ß-Gal, senescence phenotype

Mol. Cells
Sep 30, 2022 Vol.45 No.9, pp. 603~672
COVER PICTURE
The Target of Rapamycin Complex (TORC) is a central regulatory hub in eukaryotes, which is well conserved in diverse plant species, including tomato (Solanum lycopersicum). Inhibition of TORC genes (SlTOR, SlLST8, and SlRAPTOR) by VIGS (virus-induced gene silencing) results in early fruit ripening in tomato. The red/ orange tomatoes are early-ripened TORC-silenced fruits, while the green tomato is a control fruit. Top, left, control fruit (TRV2-myc); top, right, TRV2-SlLST8; bottom, left, TRV2-SlTOR; bottom, right, TRV2-SlRAPTOR(Choi et al., pp. 660-672).

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