» Articles » PMID: 20308090

The Population Genetics of Mutations: Good, Bad and Indifferent

Overview
Specialty Biology
Date 2010 Mar 24
PMID 20308090
Citations 93
Authors
Affiliations
Soon will be listed here.
Abstract

Population genetics is fundamental to our understanding of evolution, and mutations are essential raw materials for evolution. In this introduction to more detailed papers that follow, we aim to provide an oversight of the field. We review current knowledge on mutation rates and their harmful and beneficial effects on fitness and then consider theories that predict the fate of individual mutations or the consequences of mutation accumulation for quantitative traits. Many advances in the past built on models that treat the evolution of mutations at each DNA site independently, neglecting linkage of sites on chromosomes and interactions of effects between sites (epistasis). We review work that addresses these limitations, to predict how mutations interfere with each other. An understanding of the population genetics of mutations of individual loci and of traits affected by many loci helps in addressing many fundamental and applied questions: for example, how do organisms adapt to changing environments, how did sex evolve, which DNA sequences are medically important, why do we age, which genetic processes can generate new species or drive endangered species to extinction, and how should policy on levels of potentially harmful mutagens introduced into the environment by humans be determined?

Citing Articles

The Global Challenge of : Antimicrobial Resistance and Emerging Intervention Strategies.

Bukari Z, Emmanuel T, Woodward J, Ferguson R, Ezughara M, Darga N Trop Med Infect Dis. 2025; 10(1).

PMID: 39852676 PMC: 11768457. DOI: 10.3390/tropicalmed10010025.


What can we infer about mutation calling by using time-series mutation accumulation data and a Bayesian Mutation Finder?.

Maruki T, Ozere A, Freeman J, Cristescu M Ecol Evol. 2024; 14(11):e70339.

PMID: 39524312 PMC: 11550904. DOI: 10.1002/ece3.70339.


Thyroid Malignancy and Cutaneous Lichen Amyloidosis: Key Points Amid Pathogenic Variants in Medullary Thyroid Cancer/Multiple Endocrine Neoplasia Type 2 (MEN2).

Stanescu L, Ghemigian A, Ciobica M, Nistor C, Ciuche A, Radu A Int J Mol Sci. 2024; 25(18).

PMID: 39337252 PMC: 11431960. DOI: 10.3390/ijms25189765.


Embodied Computational Evolution: A Model for Investigating Randomness and the Evolution of Morphological Complexity.

Aaron E, Long Jr J Integr Org Biol. 2024; 6(1):obae032.

PMID: 39309481 PMC: 11413536. DOI: 10.1093/iob/obae032.


Exploring the promise of regulator of G Protein Signaling 20: insights into potential mechanisms and prospects across solid cancers and hematological malignancies.

Wang Y, Qin J, Sharma A, Dakal T, Wang J, Pan T Cancer Cell Int. 2024; 24(1):305.

PMID: 39227952 PMC: 11373255. DOI: 10.1186/s12935-024-03487-y.


References
1.
Rouzine I, Brunet E, Wilke C . The traveling-wave approach to asexual evolution: Muller's ratchet and speed of adaptation. Theor Popul Biol. 2007; 73(1):24-46. PMC: 2246079. DOI: 10.1016/j.tpb.2007.10.004. View

2.
Loewe L . Quantifying the genomic decay paradox due to Muller's ratchet in human mitochondrial DNA. Genet Res. 2006; 87(2):133-59. DOI: 10.1017/S0016672306008123. View

3.
Mackay T, Fry J, Lyman R, Nuzhdin S . Polygenic mutation in Drosophila melanogaster: estimates from response to selection of inbred strains. Genetics. 1994; 136(3):937-51. PMC: 1205898. DOI: 10.1093/genetics/136.3.937. View

4.
Nagylaki T . The evolution of multilocus systems under weak selection. Genetics. 1993; 134(2):627-47. PMC: 1205503. DOI: 10.1093/genetics/134.2.627. View

5.
Lynch M, Hill W . PHENOTYPIC EVOLUTION BY NEUTRAL MUTATION. Evolution. 2017; 40(5):915-935. DOI: 10.1111/j.1558-5646.1986.tb00561.x. View