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BioArchitecture Volume 4, 2014 - Issue 6
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Commentary

Imperfect asymmetry: The mechanism governing asymmetric partitioning of damaged cellular components during mitosis

Sundararaghavan PattabiramanDepartment of Cell and Developmental Biology; Alexander Silberman Institute of Life Sciences; Hebrew University of Jerusalem; Jerusalem, Israel
&
Daniel KaganovichDepartment of Cell and Developmental Biology; Alexander Silberman Institute of Life Sciences; Hebrew University of Jerusalem; Jerusalem, IsraelCorrespondence[email protected]
Pages 203-209 | Received 19 Jan 2015, Accepted 26 Jan 2015, Published online: 22 May 2015

Figures & data

Figure 1. (A) 3D time-lapse (4D imaging) of a live neuronal-derived cell line entering asymmetric mitosis. Vimentin IF is red, Histone-2b is blue, alpha-Tubulin is green and F-Actin is white. Misfolded proteins in the collapsed VIF JUNQ are inherited by the aging cell. (B) Model of VIF attachment to aging determinants, including stress foci (misfolded proteins), p-bodies (RNA), stress granules (RNA), and old mitochondria. (C) Model of asymmetric inheritance of collapsed VIF during mitosis. Cells which avoid inheriting collapsed VIF, which traps aging determinants, are more youthful and rejuvenated.

Figure 1. (A) 3D time-lapse (4D imaging) of a live neuronal-derived cell line entering asymmetric mitosis. Vimentin IF is red, Histone-2b is blue, alpha-Tubulin is green and F-Actin is white. Misfolded proteins in the collapsed VIF JUNQ are inherited by the aging cell. (B) Model of VIF attachment to aging determinants, including stress foci (misfolded proteins), p-bodies (RNA), stress granules (RNA), and old mitochondria. (C) Model of asymmetric inheritance of collapsed VIF during mitosis. Cells which avoid inheriting collapsed VIF, which traps aging determinants, are more youthful and rejuvenated.

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