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'''Bacterial senescence''' or '''bacterial aging''' refers to the gradual decrease in [[Cell (biology)|cellular]] function in individual [[bacterium]] as they increase in age. Indicators of senescence include a decelerated division rate and an increase likelihood of death.
'''Bacterial senescence''' or '''bacterial aging''' refers to the gradual decrease in [[Cell (biology)|cellular]] function in individual [[bacterium]] as they increase in age. Indicators of senescence include a decelerated division rate and an increase likelihood of death.


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.<ref>Ackermann, M., Stearns, S. C., & Jenal, U. (2003). Senescence in a bacterium with asymmetric division. Science (New York, N.Y.), 300(5627), 1920–1920. doi:10.1126/science.1083532</ref> Recent evidence also shows that the symmetrically dividing bacteria, Escherichia ''coli'', exhibit signs of replicative aging caused by subtle asymmetries in its division.<ref>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</ref><ref>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. doi:10.1073/pnas.0708931105</ref>
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.<ref>{{cite journal | last1 = Ackermann | first1 = M. | last2 = Stearns | first2 = S. C. | last3 = Jenal | first3 = U. | year = 2003 | title = Senescence in a bacterium with asymmetric division | url = | journal = Science | volume = 300 | issue = 5627| pages = 1920–1920 | doi = 10.1126/science.1083532 }}</ref> Recent evidence also shows that the symmetrically dividing bacteria, Escherichia ''coli'', exhibit signs of replicative aging caused by subtle asymmetries in its division.<ref>{{cite journal | last1 = Stewart | first1 = E. J. | last2 = Madden | first2 = R. | last3 = Paul | first3 = G. | last4 = Taddei | first4 = F. | year = 2005 | title = Aging and Death in an Organism That Reproduces by Morphologically Symmetric Division | url = | journal = PLoS Biology | volume = 3 | issue = 2| page = e45 | doi = 10.1371/journal.pbio.0030045 }}</ref><ref>{{cite journal | last1 = Lindner | first1 = A. B. | last2 = Madden | first2 = R. | last3 = Demarez | first3 = A. | last4 = Stewart | first4 = E. J. | last5 = Taddei | first5 = F. | year = 2008 | title = Asymmetric segregation of protein aggregates is associated with cellular aging and rejuvenation | url = | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 105 | issue = 8| pages = 3076–3081 | doi = 10.1073/pnas.0708931105 }}</ref>


== Factors contributing to aging==
== 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.<br />
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.<br />
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.<ref>{{Cite journal|url = http://www.pnas.org/content/103/40/14831.full|title = Aging may be a conditional strategic choice and not an inevitable outcome for bacteria|last = Watve|first = Milind|date = October 2006|journal = Proceedings of the National Academy of Sciences of the United States of America|accessdate = |doi = 10.1073/pnas.0606499103 }}</ref><ref>Kirkwood, T. B. L. (1981). Repair and its evolution: survival versus reproduction. Physiological Ecology ; an Evolutionary Approach to Resource Use.</ref> The single celled eukaryotic organism, Sacchoaromyces ''cerevisiae'', retains deleterious aging factors in the mother cell leading to rejuvenation of the daughter.<ref>Aguilaniu, H., Gustafsson, L., Rigoulet, M., & Nystroem, T. (2003). Asymmetric inheritance of oxidatively damaged proteins during cytokinesis. Science (New York, N.Y.), 299(5613), 1751–1753. doi:10.1126/science.1080418</ref>
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.<ref>{{Cite journal|url = http://www.pnas.org/content/103/40/14831.full|title = Aging may be a conditional strategic choice and not an inevitable outcome for bacteria|last = Watve|first = Milind|date = October 2006|journal = Proceedings of the National Academy of Sciences of the United States of America|accessdate = |doi = 10.1073/pnas.0606499103 }}</ref><ref>Kirkwood, T. B. L. (1981). Repair and its evolution: survival versus reproduction. Physiological Ecology ; an Evolutionary Approach to Resource Use.</ref> The single celled eukaryotic organism, Sacchoaromyces ''cerevisiae'', retains deleterious aging factors in the mother cell leading to rejuvenation of the daughter.<ref>{{cite journal | last1 = Aguilaniu | first1 = H. | last2 = Gustafsson | first2 = L. | last3 = Rigoulet | first3 = M. | last4 = Nystroem | first4 = T. | year = 2003 | title = Asymmetric inheritance of oxidatively damaged proteins during cytokinesis | url = | journal = Science | volume = 299 | issue = 5613| pages = 1751–1753 | doi = 10.1126/science.1080418 }}</ref>


==Aging in Asymmetrically dividing Bacteria==
==Aging in Asymmetrically dividing Bacteria==
A well established example of bacterial aging is Caulobacter crescentus. This bacteria 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 stalked cell then becomes reproductively active and gives rise to new swarmer cells. The number of progeny produced per hour by individual swarmer cells was shown to decrease with age.<ref>Ackermann, M., Stearns, S. C., & Jenal, U. (2003). Senescence in a bacterium with asymmetric division. Science (New York, N.Y.), 300(5627), 1920–1920. doi:10.1126/science.1083532</ref> This was the first evidence of bacterial aging.<ref>Nystroem, T. (2007). A bacterial kind of aging. Plos Genetics, 3(12), 2355–2357. doi:10.1371/journal.pgen.0030224</ref>
A well established example of bacterial aging is Caulobacter crescentus. This bacteria 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 stalked cell then becomes reproductively active and gives rise to new swarmer cells. The number of progeny produced per hour by individual swarmer cells was shown to decrease with age.<ref>{{cite journal | last1 = Ackermann | first1 = M. | last2 = Stearns | first2 = S. C. | last3 = Jenal | first3 = U. | year = 2003 | title = Senescence in a bacterium with asymmetric division | url = | journal = Science | volume = 300 | issue = 5627| pages = 1920–1920 | doi = 10.1126/science.1083532 }}</ref> This was the first evidence of bacterial aging.<ref>{{cite journal | last1 = Nystroem | first1 = T | year = 2007 | title = A bacterial kind of aging | url = | journal = Plos Genetics | volume = 3 | issue = 12| pages = 2355–2357 | doi = 10.1371/journal.pgen.0030224 }}</ref>


==Aging in Symmetrically dividing Bacteria==
==Aging in Symmetrically dividing Bacteria==
Organisms which replicate via symmetric division, such as E. ''coli'', are thought to be immortal.<ref>Moseley, J. B. (2013). Cellular Aging: Symmetry Evades Senescence. Current Biology, 23(19), R871–R873. doi:10.1016/j.cub.2013.08.013</ref> 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.<ref>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</ref> This has been refuted by Wang. el al, in which individual E. ''coli'' were shown to have a consistent growth rate decoupled from cell death, which was instead the result of stochastic filamentation and SOS response.<ref>{{cite journal |quotes= |last=Wang |first=Ping |authorlink= |author2=Lydia Robert |author3=James Pelletier |author4=Wei Lien Dang |author5=Francois Taddei |author6=Andrew Wright |author7=Suckjoon Jun |year=2010 |title=Robust Growth of E. coli |journal=Current Biology |volume=20 |issue=12 |pages=1099–103 |doi=10.1016/j.cub.2010.04.045 |id= |url= http://www.cell.com/current-biology/abstract/S0960-9822(10)00524-5 |accessdate=November 12, 2014 |pmid= 20537537 |pmc=2902570 }}</ref> This discrepancy may be due to the different culturing methods used in the studies, i.e. growth on agar pads vs. inside a microfludic device, for which [[quorum sensing]] exists in the former, but is absent in the latter.
Organisms which replicate via symmetric division, such as E. ''coli'', are thought to be immortal.<ref>{{cite journal | last1 = Moseley | first1 = J. B. | year = 2013 | title = Cellular Aging: Symmetry Evades Senescence | url = | journal = Current Biology | volume = 23 | issue = 19| pages = R871–R873 | doi = 10.1016/j.cub.2013.08.013 }}</ref> 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.<ref>{{cite journal | last1 = Stewart | first1 = E. J. | last2 = Madden | first2 = R. | last3 = Paul | first3 = G. | last4 = Taddei | first4 = F. | year = 2005 | title = Aging and Death in an Organism That Reproduces by Morphologically Symmetric Division | url = | journal = PLoS Biology | volume = 3 | issue = 2| page = e45 | doi = 10.1371/journal.pbio.0030045 }}</ref> This has been refuted by Wang. el al, in which individual E. ''coli'' were shown to have a consistent growth rate decoupled from cell death, which was instead the result of stochastic filamentation and SOS response.<ref>{{cite journal |quotes= |last=Wang |first=Ping |authorlink= |author2=Lydia Robert |author3=James Pelletier |author4=Wei Lien Dang |author5=Francois Taddei |author6=Andrew Wright |author7=Suckjoon Jun |year=2010 |title=Robust Growth of E. coli |journal=Current Biology |volume=20 |issue=12 |pages=1099–103 |doi=10.1016/j.cub.2010.04.045 |id= |url= http://www.cell.com/current-biology/abstract/S0960-9822(10)00524-5 |accessdate=November 12, 2014 |pmid= 20537537 |pmc=2902570 }}</ref> This discrepancy may be due to the different culturing methods used in the studies, i.e. growth on agar pads vs. inside a microfludic device, for which [[quorum sensing]] exists in the former, but is absent in the latter.


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.<ref>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. doi:10.1073/pnas.0708931105</ref> 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.<ref>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). doi:10.1371/journal.pcbi.1003038</ref> A similar mechanism of aging has been found to occur in Schizosaccharomyces Pombe, which divides via symmetrical binary fission.<ref>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.</ref>
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.<ref>{{cite journal | last1 = Lindner | first1 = A. B. | last2 = Madden | first2 = R. | last3 = Demarez | first3 = A. | last4 = Stewart | first4 = E. J. | last5 = Taddei | first5 = F. | year = 2008 | title = Asymmetric segregation of protein aggregates is associated with cellular aging and rejuvenation | url = | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 105 | issue = 8| pages = 3076–3081 | doi = 10.1073/pnas.0708931105 }}</ref> 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.<ref>{{cite journal | last1 = Coquel | first1 = A.-S. | last2 = Jacob | first2 = J.-P. | last3 = Primet | first3 = M. | last4 = Demarez | first4 = A. | last5 = Dimiccoli | first5 = M. | last6 = Julou | first6 = T. | display-authors = 6 | last7 = et al | year = 2013 | title = Localization of Protein Aggregation in Escherichia coli Is Governed by Diffusion and Nucleoid Macromolecular Crowding Effect | url = | journal = PLOS Computational Biology | volume = 9 | issue = | page = 4 | doi = 10.1371/journal.pcbi.1003038 }}</ref> A similar mechanism of aging has been found to occur in Schizosaccharomyces Pombe, which divides via symmetrical binary fission.<ref>{{cite journal | last1 = Coelho | first1 = M. | last2 = Dereli | first2 = A. | last3 = Haese | first3 = A. | last4 = Kühn | first4 = S. | last5 = Malinovska | first5 = L. | year = 2013 | title = Fission yeast does not age under favorable conditions, but does so after stress | url = | journal = Current Biology | volume = | issue = | page = }}</ref>


==References==
==References==

Revision as of 16:01, 13 December 2014

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

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.[1] Recent evidence also shows that the symmetrically dividing bacteria, Escherichia coli, exhibit signs of replicative aging caused by subtle asymmetries in its division.[2][3]

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.[4][5] The single celled eukaryotic organism, Sacchoaromyces cerevisiae, retains deleterious aging factors in the mother cell leading to rejuvenation of the daughter.[6]

Aging in Asymmetrically dividing Bacteria

A well established example of bacterial aging is Caulobacter crescentus. This bacteria 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 stalked cell then becomes reproductively active and gives rise to new swarmer cells. The number of progeny produced per hour by individual swarmer cells was shown to decrease with age.[7] This was the first evidence of bacterial aging.[8]

Aging in Symmetrically dividing Bacteria

Organisms which replicate via symmetric division, such as E. coli, are thought to be immortal.[9] 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.[10] This has been refuted by Wang. el al, in which individual E. coli were shown to have a consistent growth rate decoupled from cell death, which was instead the result of stochastic filamentation and SOS response.[11] This discrepancy may be due to the different culturing methods used in the studies, i.e. growth on agar pads vs. inside a microfludic device, for which quorum sensing exists in the former, but is absent in the latter.

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.[12] 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.[13] A similar mechanism of aging has been found to occur in Schizosaccharomyces Pombe, which divides via symmetrical binary fission.[14]

References

  1. ^ Ackermann, M.; Stearns, S. C.; Jenal, U. (2003). "Senescence in a bacterium with asymmetric division". Science. 300 (5627): 1920–1920. doi:10.1126/science.1083532.
  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.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ 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. doi:10.1073/pnas.0708931105.
  4. ^ Watve, Milind (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. doi:10.1073/pnas.0606499103.
  5. ^ Kirkwood, T. B. L. (1981). Repair and its evolution: survival versus reproduction. Physiological Ecology ; an Evolutionary Approach to Resource Use.
  6. ^ Aguilaniu, H.; Gustafsson, L.; Rigoulet, M.; Nystroem, T. (2003). "Asymmetric inheritance of oxidatively damaged proteins during cytokinesis". Science. 299 (5613): 1751–1753. doi:10.1126/science.1080418.
  7. ^ Ackermann, M.; Stearns, S. C.; Jenal, U. (2003). "Senescence in a bacterium with asymmetric division". Science. 300 (5627): 1920–1920. doi:10.1126/science.1083532.
  8. ^ Nystroem, T (2007). "A bacterial kind of aging". Plos Genetics. 3 (12): 2355–2357. doi:10.1371/journal.pgen.0030224.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  9. ^ Moseley, J. B. (2013). "Cellular Aging: Symmetry Evades Senescence". Current Biology. 23 (19): R871–R873. doi:10.1016/j.cub.2013.08.013.
  10. ^ 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.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  11. ^ 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. Retrieved November 12, 2014. {{cite journal}}: Cite has empty unknown parameter: |quotes= (help)
  12. ^ 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. doi:10.1073/pnas.0708931105.
  13. ^ 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. doi:10.1371/journal.pcbi.1003038. {{cite journal}}: Explicit use of et al. in: |last7= (help)CS1 maint: unflagged free DOI (link)
  14. ^ 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.
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