#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

A Model for Damage Load and Its Implications for the Evolution of Bacterial Aging


Deleterious mutations appearing in a population increase in frequency until stopped by natural selection. The ensuing equilibrium creates a stable frequency of deleterious mutations or the mutational load. Here I develop the comparable concept of a damage load, which is caused by harmful non-heritable changes to the phenotype. A damage load also ensues when the increase of damage is opposed by selection. The presence of a damage load favors the evolution of asymmetrical transmission of damage by a mother to her daughters. The asymmetry is beneficial because it increases fitness variance, but it also leads to aging or senescence. A mathematical model based on microbes reveals that a cell lineage dividing symmetrically is immortal if lifetime damage rates do not exceed a threshold. The evolution of asymmetry allows the lineage to persist above the threshold, but the lineage becomes mortal. In microbes with low genomic mutation rates, it is likely that the damage load is much greater than the mutational load. In metazoans with higher genomic mutation rates, the damage and the mutational load could be of the same magnitude. A fit of the model to experimental data shows that Escherichia coli cells experience a damage rate that is below the threshold and are immortal under the conditions examined. The model estimates the asymmetry level of E. coli to be low but sufficient for persisting at higher damage rates. The model also predicts that increasing asymmetry results in diminishing fitness returns, which may explain why the bacterium has not evolved higher asymmetry.


Vyšlo v časopise: A Model for Damage Load and Its Implications for the Evolution of Bacterial Aging. PLoS Genet 6(8): e32767. doi:10.1371/journal.pgen.1001076
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.pgen.1001076

Souhrn

Deleterious mutations appearing in a population increase in frequency until stopped by natural selection. The ensuing equilibrium creates a stable frequency of deleterious mutations or the mutational load. Here I develop the comparable concept of a damage load, which is caused by harmful non-heritable changes to the phenotype. A damage load also ensues when the increase of damage is opposed by selection. The presence of a damage load favors the evolution of asymmetrical transmission of damage by a mother to her daughters. The asymmetry is beneficial because it increases fitness variance, but it also leads to aging or senescence. A mathematical model based on microbes reveals that a cell lineage dividing symmetrically is immortal if lifetime damage rates do not exceed a threshold. The evolution of asymmetry allows the lineage to persist above the threshold, but the lineage becomes mortal. In microbes with low genomic mutation rates, it is likely that the damage load is much greater than the mutational load. In metazoans with higher genomic mutation rates, the damage and the mutational load could be of the same magnitude. A fit of the model to experimental data shows that Escherichia coli cells experience a damage rate that is below the threshold and are immortal under the conditions examined. The model estimates the asymmetry level of E. coli to be low but sufficient for persisting at higher damage rates. The model also predicts that increasing asymmetry results in diminishing fitness returns, which may explain why the bacterium has not evolved higher asymmetry.


Zdroje

1. HaldaneJBS

1937 The Effect of Variation of Fitness. The American Naturalist 71 337 349

2. KondrashovAS

1993 Classification of Hypotheses on the Advantage of Amphimixis. Journal of Heredity 84 372 387

3. MullerHJ

1950 Our Load of Mutations. American Journal of Human Genetics 2 111 176

4. CrowJF

1958 Some possibilities for measuring -selection intensities in man. Human Biol 30 1 13

5. KimuraM

MaruyamaT

1966 Mutational Load with Epistatic Gene Interactions in Fitness. Genetics 54 1337 1351

6. OhtaT

1973 Slightly Deleterious Mutant Substitutions in Evolution. Nature 246 96 98

7. CharlesworthB

CharlesworthD

1998 Some evolutionary consequences of deleterious mutations. Genetica 103 3 19

8. AckermannM

ChaoL

BergstromCT

DoebeliM

2007 On the evolutionary origin of aging. Aging Cell 6 235 244

9. EvansSN

SteinsaltzD

2007 Damage segregation at fissioning may increase growth rates: A superprocess model. Theoretical Population Biology 71 473 490

10. WatveM

ParabS

JogdandP

KeniS

2006 Aging may be a conditional strategic choice and not an inevitable outcome for bacteria. Proc Natl Acad Sci U S A 103 14831 14835

11. ErjavecN

CvijovicM

KlippE

NystromT

2008 Selective benefits of damage partitioning in unicellular systems and its effects on aging. Proc Natl Acad Sci U S A 105 18764 18769

12. AckermannM

StearnsSC

JenalU

2003 Senescence in a bacterium with asymmetric division. Science 300 1920 1920

13. LindnerAB

MaddenR

DemarezA

StewartEJ

TaddeiF

2008 Asymmetric segregation of protein aggregates is associated with cellular aging and rejuvenation. Proc Natl Acad Sci U S A 105 3076 3081

14. StewartEJ

MaddenR

PaulG

TaddeiF

2005 Aging and death in an organism that reproduces by morphologically symmetric division. Plos Biology 3 e45 doi:10.1371/journal.pbio.0030045

15. BoyeE

NordstromK

2003 Coupling the cell cycle to cell growth - A look at the parameters that regulate cell-cycle events. Embo Reports 4 757 760

16. VinellaD

DariR

1995 Overview of Controls in the Escherichia-Coli Cell-Cycle. Bioessays 17 527 536

17. PondSLK

FrostSDW

MuseSV

2005 HyPhy: hypothesis testing using phylogenies. Bioinformatics 21 676 679

18. O'DonaldP

1968 Measuring the intensity of natural selection. Nature 220 197 198

19. KirkwoodTB

2005 Asymmetry and the origins of ageing. Mech Ageing Dev 126 533 534

20. FerberD

2005 Microbiology. Immortality dies as bacteria show their age. Science 307 656

21. NystromT

2002 Aging in bacteria. Curr Opin Microbiol 5 596 601

22. WoldringhCL

2005 Is Escherichia coli getting old? Bioessays 27 770 774

23. StewartE

TaddeiF

2005 Aging in Esherichia coli: signals in the noise. Bioessays 27 983

24. CharnovEL

1976 Optimal Foraging, Marginal Value Theorem. Theoretical Population Biology 9 129 136

25. GrossL

2007 Paradox Resolved? The Strange Case of the Radiation-Resistant Bacteria. PLoS Biology 5 e108 doi:10.1371/journal.pbio.0050108

26. LambethJD

2004 NOX enzymes and the biology of reactive oxygen. Nat Rev Immunol 4 181 189

27. ParkB

NizetV

LiuGY

2008 Role of Staphylococcus aureus catalase in niche competition against Streptococcus pneumoniae. J Bacteriol 190 2275 2278

28. DukanS

FarewellA

BallesterosM

TaddeiF

RadmanM

2000 Protein oxidation in response to increased transcriptional or translational errors. Proc Natl Acad Sci U S A 97 5746 5749

29. DokeN

MiuraY

SanchezLM

ParkHJ

NoritakeT

1996 The oxidative burst protects plants against pathogen attack: mechanism and role as an emergency signal for plant bio-defence–a review. Gene 179 45 51

30. DesnuesB

CunyC

GregoriG

DukanS

AguilaniuH

2003 Differential oxidative damage and expression of stress defence regulons in culturable and non-culturable Escherichia coli cells. EMBO Rep 4 400 404

31. KirkwoodTB

2005 Understanding the odd science of aging. Cell 120 437 447

32. TurkePW

2008 Williams's theory of the evolution of senescence: Still useful at fifty. Quarterly Review of Biology 83 243 256

33. DrakeJW

CharlesworthB

CharlesworthD

CrowJF

1998 Rates of spontaneous mutation. Genetics 148 1667 1686

34. MayRM

1976 Simple Mathematical-Models with Very Complicated Dynamics. Nature 261 459 467

Štítky
Genetika Reprodukčná medicína

Článok vyšiel v časopise

PLOS Genetics


2010 Číslo 8
Najčítanejšie tento týždeň
Najčítanejšie v tomto čísle
Kurzy

Zvýšte si kvalifikáciu online z pohodlia domova

Aktuální možnosti diagnostiky a léčby litiáz
nový kurz
Autori: MUDr. Tomáš Ürge, PhD.

Všetky kurzy
Prihlásenie
Zabudnuté heslo

Zadajte e-mailovú adresu, s ktorou ste vytvárali účet. Budú Vám na ňu zasielané informácie k nastaveniu nového hesla.

Prihlásenie

Nemáte účet?  Registrujte sa

#ADS_BOTTOM_SCRIPTS#