Bacterial senescence or bacterial aging refers to the gradual decrease in cellular function in individual bacteria as they increase in age. Indicators of senescence include a decelerated division rate and an increase likelihood of death.[1]

The fundamental cause of aging in bacteria is thought to be the accumulation of deleterious components (aging factors). Asymmetrically dividing bacteria, such as Caulobacter crescentus, show signs of replicative aging.[2] The results for symmetrically dividing bacteria are more nuanced. For example, Escherichia coli, under certain experimental conditions, may exhibit signs of replicative aging caused by subtle asymmetries in its division.[3][4][5]

Factors contributing to aging

Aging factors can be defined as irreparable damages to cellular components which ultimately contribute to the decreased fitness of the individual harbouring them. Putative aging factors include damaged DNA strands, old cell-surface material, and mis-folded or aggregated protein. The cell poles of replicating E. coli are often used as a proxy for aging factors as each bacterium inherits an old cell-pole (mother's pole) and a newly synthesized new cell-pole. Inclusion bodies, masses of aggregated damaged or mis-folded proteins, have recently been shown to contribute to the aging of cellular organisms.

Senescence in single celled organisms is thought to arise via the asymmetric partitioning of aging factors between daughter cells. It has long been argued that, on theoretical grounds, the preferential segregation of damage in unicellular organisms would contribute to the fitness of the overall population.[6][7] The single celled eukaryotic organism, Saccharomyces cerevisiae, retains deleterious aging factors in the mother cell leading to rejuvenation of the daughter.[8]

Aging in asymmetrically dividing bacteria

A well-established example of bacterial aging is Caulobacter crescentus. This bacterium begins its life as a motile swarmer cell. Once it has found a suitable substrate, the swarmer cell will differentiate into a non-motile stalked cell.The asymmetrically dividing cells then show signs of detrimental genetic variation as they divide.[9] The stalked cell then becomes reproductively active and gives rise to new swarmer cells. The number of progenies produced per hour by individual swarmer cells was shown to decrease with age.[2] This was the first evidence of bacterial aging.[10] Aging in asymmetrically dividing bacteria could also be due to the division of cell damage in the cell fission stage increasing the damage in one cell and purging it in another.[11] This is also true for B.subtilis the asymmetric cell division generates two cells that contain different regulatory proteins and express different fates one becomes of the daughters becoming able to transcript and the other cannot.[12]

Aging in symmetrically dividing bacteria

Organisms which replicate via symmetric division, such as E. coli, are thought to be immortal.[13] However, by tracking the inheritance of both the new and old cell pole, evidence of aging was found in E. coli. A cell which has consecutively inherited the old cell pole has been shown to exhibit a significantly decreased growth rate.[3] The decline in growth rate in Stewart et al. appears to be at least partially attributed to the preferential localization of inclusion bodies near the old cell wall.[4] This localization is thought to be the passive result of the slow diffusion of the large aggregate, and the exclusion of the aggregate by the nucleoid.[14] A similar mechanism of aging has been found to occur in Schizosaccharomyces pombe, which divides via symmetrical binary fission.[15] Mutations in the cells did not show any signs of aging with respect to growth in the symmetrically dividing E.Coli until the cells with deficient repair enzymes and an increased number of mutations caused the growth rate to decrease, the repair-deficient cells reduced growth in a stepwise manner which suggest that single mutations can cause a growth reduction or can cease growth completely which caused the bacteria die.

[16]

However, the original findings of E. coli aging have been partially refuted by more recent microfluidics-based studies, in which individual E. coli showed a constant growth rate for hundreds of consecutive cell divisions, although the death rate increased in each cell division.[5] This discrepancy may be due to the different culturing methods used in the two studies, i.e., growth on agar pads vs. in a microfluidic device.[17]

See also

References

  1. ↑ Nyström, Thomas (2003-03-25). "Conditional senescence in bacteria: death of the immortals: Bacterial senescence". Molecular Microbiology. 48 (1): 17–23. doi:10.1046/j.1365-2958.2003.03385.x. PMID 12657042. S2CID 35548948.
  2. 1 2 Ackermann, M.; Stearns, S. C.; Jenal, U. (2003). "Senescence in a bacterium with asymmetric division". Science. 300 (5627): 1920. doi:10.1126/science.1083532. PMID 12817142. S2CID 34770745.
  3. 1 2 Stewart, E. J.; Madden, R.; Paul, G.; Taddei, F. (2005). "Aging and Death in an Organism That Reproduces by Morphologically Symmetric Division". PLOS Biology. 3 (2): e45. doi:10.1371/journal.pbio.0030045. PMC 546039. PMID 15685293.
  4. 1 2 Lindner, A. B.; Madden, R.; Demarez, A.; Stewart, E. J.; Taddei, F. (2008). "Asymmetric segregation of protein aggregates is associated with cellular aging and rejuvenation". Proceedings of the National Academy of Sciences of the United States of America. 105 (8): 3076–3081. Bibcode:2008PNAS..105.3076L. doi:10.1073/pnas.0708931105. PMC 2268587. PMID 18287048.
  5. 1 2 Wang, Ping; Lydia Robert; James Pelletier; Wei Lien Dang; Francois Taddei; Andrew Wright; Suckjoon Jun (2010). "Robust Growth of E. coli". Current Biology. 20 (12): 1099–103. doi:10.1016/j.cub.2010.04.045. PMC 2902570. PMID 20537537.
  6. ↑ Watve, Milind; Parab, S.; Jogdand, P.; Keni, S. (October 2006). "Aging may be a conditional strategic choice and not an inevitable outcome for bacteria". Proceedings of the National Academy of Sciences of the United States of America. 103 (40): 14831–5. Bibcode:2006PNAS..10314831W. doi:10.1073/pnas.0606499103. PMC 1595437. PMID 17001004.
  7. ↑ Kirkwood, T. B. L. (1981). Repair and its evolution: survival versus reproduction. Physiological Ecology ; an Evolutionary Approach to Resource Use.
  8. ↑ Aguilaniu, H.; Gustafsson, L.; Rigoulet, M.; Nystroem, T. (2003). "Asymmetric inheritance of oxidatively damaged proteins during cytokinesis". Science. 299 (5613): 1751–1753. Bibcode:2003Sci...299.1751A. doi:10.1126/science.1080418. PMID 12610228. S2CID 21337636.
  9. ↑ Kohn, Michael H.; Murphy, William J.; Ostrander, Elaine A.; Wayne, Robert K. (2006-11-01). "Genomics and conservation genetics". Trends in Ecology & Evolution. 21 (11): 629–637. doi:10.1016/j.tree.2006.08.001. ISSN 0169-5347. PMID 16908089.
  10. ↑ Nystroem, T (2007). "A bacterial kind of aging". PLOS Genetics. 3 (12): 2355–2357. doi:10.1371/journal.pgen.0030224. PMC 2134940. PMID 18085827.
  11. ↑ Steiner, Ulrich Karl (2021). "Senescence in Bacteria and Its Underlying Mechanisms". Frontiers in Cell and Developmental Biology. 9: 668915. doi:10.3389/fcell.2021.668915. ISSN 2296-634X. PMC 8249858. PMID 34222238.
  12. ↑ Way, J. C. (February 1996). "The mechanism of bacterial asymmetric cell division". BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology. 18 (2): 99–101. doi:10.1002/bies.950180205. ISSN 0265-9247. PMID 8851042.
  13. ↑ Moseley, J. B. (2013). "Cellular Aging: Symmetry Evades Senescence". Current Biology. 23 (19): R871–R873. doi:10.1016/j.cub.2013.08.013. PMC 4276399. PMID 24112980.
  14. ↑ Coquel, A.-S.; Jacob, J.-P.; Primet, M.; Demarez, A.; Dimiccoli, M.; Julou, T.; et al. (2013). "Localization of Protein Aggregation in Escherichia coli Is Governed by Diffusion and Nucleoid Macromolecular Crowding Effect". PLOS Computational Biology. 9 (4): 4. arXiv:1303.1904. Bibcode:2013PLSCB...9E3038C. doi:10.1371/journal.pcbi.1003038. PMC 3636022. PMID 23633942.
  15. ↑ Coelho, M.; Dereli, A.; Haese, A.; Kühn, S.; Malinovska, L. (2013). "Fission yeast does not age under favorable conditions, but does so after stress". Current Biology. 23 (19): 1844–52. doi:10.1016/j.cub.2013.07.084. PMC 4620659. PMID 24035542.
  16. ↑ Robert, Lydia; Ollion, Jean; Robert, Jerome; Song, Xiaohu; Matic, Ivan; Elez, Marina (2018-03-16). "Mutation dynamics and fitness effects followed in single cells". Science. 359 (6381): 1283–1286. doi:10.1126/science.aan0797. ISSN 0036-8075. PMID 29590079. S2CID 4548806.
  17. ↑ Proenca, Audrey Menegaz; Rang, Camilla Ulla; Qiu, Andrew; Shi, Chao; Chao, Lin (2019-05-23). "Cell aging preserves cellular immortality in the presence of lethal levels of damage". PLOS Biology. 17 (5): e3000266. doi:10.1371/journal.pbio.3000266. ISSN 1545-7885. PMC 6532838. PMID 31120870.
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