Cell aging preserves cellular immortality in the presence of lethal levels of damage.
Cellular aging, a progressive functional decline driven by damage accumulation, often culminates in the mortality of a cell lineage. Certain lineages, however, are able to sustain long-lasting immortality, as prominently exemplified by stem cells. Here, we show that Escherichia coli cell lineages ex...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2019-05-01
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| Series: | PLoS Biology |
| Online Access: | https://doi.org/10.1371/journal.pbio.3000266 |
| _version_ | 1830188415259246592 |
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| author | Audrey Menegaz Proenca Camilla Ulla Rang Andrew Qiu Chao Shi Lin Chao |
| author_facet | Audrey Menegaz Proenca Camilla Ulla Rang Andrew Qiu Chao Shi Lin Chao |
| author_sort | Audrey Menegaz Proenca |
| collection | DOAJ |
| description | Cellular aging, a progressive functional decline driven by damage accumulation, often culminates in the mortality of a cell lineage. Certain lineages, however, are able to sustain long-lasting immortality, as prominently exemplified by stem cells. Here, we show that Escherichia coli cell lineages exhibit comparable patterns of mortality and immortality. Through single-cell microscopy and microfluidic techniques, we find that these patterns are explained by the dynamics of damage accumulation and asymmetric partitioning between daughter cells. At low damage accumulation rates, both aging and rejuvenating lineages retain immortality by reaching their respective states of physiological equilibrium. We show that both asymmetry and equilibrium are present in repair mutants lacking certain repair chaperones, suggesting that intact repair capacity is not essential for immortal proliferation. We show that this growth equilibrium, however, is displaced by extrinsic damage in a dosage-dependent response. Moreover, we demonstrate that aging lineages become mortal when damage accumulation rates surpass a threshold, whereas rejuvenating lineages within the same population remain immortal. Thus, the processes of damage accumulation and partitioning through asymmetric cell division are essential in the determination of proliferative mortality and immortality in bacterial populations. This study provides further evidence for the characterization of cellular aging as a general process, affecting prokaryotes and eukaryotes alike and according to similar evolutionary constraints. |
| first_indexed | 2024-12-17T22:44:17Z |
| format | Article |
| id | doaj.art-7feff0bd3a774c6eac6d0774a2ea27ff |
| institution | Directory Open Access Journal |
| issn | 1544-9173 1545-7885 |
| language | English |
| last_indexed | 2024-12-17T22:44:17Z |
| publishDate | 2019-05-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS Biology |
| spelling | doaj.art-7feff0bd3a774c6eac6d0774a2ea27ff2022-12-21T21:29:50ZengPublic Library of Science (PLoS)PLoS Biology1544-91731545-78852019-05-01175e300026610.1371/journal.pbio.3000266Cell aging preserves cellular immortality in the presence of lethal levels of damage.Audrey Menegaz ProencaCamilla Ulla RangAndrew QiuChao ShiLin ChaoCellular aging, a progressive functional decline driven by damage accumulation, often culminates in the mortality of a cell lineage. Certain lineages, however, are able to sustain long-lasting immortality, as prominently exemplified by stem cells. Here, we show that Escherichia coli cell lineages exhibit comparable patterns of mortality and immortality. Through single-cell microscopy and microfluidic techniques, we find that these patterns are explained by the dynamics of damage accumulation and asymmetric partitioning between daughter cells. At low damage accumulation rates, both aging and rejuvenating lineages retain immortality by reaching their respective states of physiological equilibrium. We show that both asymmetry and equilibrium are present in repair mutants lacking certain repair chaperones, suggesting that intact repair capacity is not essential for immortal proliferation. We show that this growth equilibrium, however, is displaced by extrinsic damage in a dosage-dependent response. Moreover, we demonstrate that aging lineages become mortal when damage accumulation rates surpass a threshold, whereas rejuvenating lineages within the same population remain immortal. Thus, the processes of damage accumulation and partitioning through asymmetric cell division are essential in the determination of proliferative mortality and immortality in bacterial populations. This study provides further evidence for the characterization of cellular aging as a general process, affecting prokaryotes and eukaryotes alike and according to similar evolutionary constraints.https://doi.org/10.1371/journal.pbio.3000266 |
| spellingShingle | Audrey Menegaz Proenca Camilla Ulla Rang Andrew Qiu Chao Shi Lin Chao Cell aging preserves cellular immortality in the presence of lethal levels of damage. PLoS Biology |
| title | Cell aging preserves cellular immortality in the presence of lethal levels of damage. |
| title_full | Cell aging preserves cellular immortality in the presence of lethal levels of damage. |
| title_fullStr | Cell aging preserves cellular immortality in the presence of lethal levels of damage. |
| title_full_unstemmed | Cell aging preserves cellular immortality in the presence of lethal levels of damage. |
| title_short | Cell aging preserves cellular immortality in the presence of lethal levels of damage. |
| title_sort | cell aging preserves cellular immortality in the presence of lethal levels of damage |
| url | https://doi.org/10.1371/journal.pbio.3000266 |
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