Measuring Mutation Rates Using the Luria-Delbrück Fluctuation Assay

2017 ◽  
pp. 21-31 ◽  
Author(s):  
Gregory I. Lang
Keyword(s):  
Mutation Rates

Do Mutation Rates Match the Kelly Criterion?

2020 ◽  
Vol 2 (1) ◽  
pp. 31
Author(s):  
Jonathan Bartlett
Keyword(s):  
Mutation Rates ◽  
Kelly Criterion

The Kelly Criterion defines an optimal betting strategy for games that have a defined risk and payoff. This letter explores the question of if this can be used as a methodology for analyzing mutation rates.

Heterogeneity of the mutation rates of influenza A viruses: isolation of mutator mutants.

1992 ◽  
Vol 66 (4) ◽  
pp. 2491-2494 ◽  
Author(s):  
P Suárez ◽  
J Valcárcel ◽  
J Ortín
Keyword(s):  
Influenza A ◽  
Mutation Rates ◽  
Influenza A Viruses

Species-Jumping Viruses Raise Core Questions about Mutation Rates

2006 ◽  
Vol 1 (6) ◽  
pp. 262-262
Author(s):  
David Holzman
Keyword(s):  
Mutation Rates ◽  
Core Questions

The Y‐STR landscape of coastal southeastern han: Forensic characteristics, haplotype analyses, mutation rates, and population genetics

2021 ◽  
Author(s):  
Haoliang Fan ◽  
Ying Zeng ◽  
Weiwei Wu ◽  
Hong Liu ◽  
Quyi Xu ◽  
...  
Keyword(s):  
Population Genetics ◽  
Mutation Rates

scholarly journals Patterns of Cell Division and the Risk of Cancer

Genetics ◽  
2003 ◽  
Vol 163 (4) ◽  
pp. 1527-1532 ◽  
Author(s):  
Steven A Frank ◽  
Yoh Iwasa ◽  
Martin A Nowak
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Basal Layer ◽  
Mutation Rates ◽  
Tissue Architecture ◽  
Cell Lineages ◽  
Cell Mutation ◽  
Long Stem ◽  
Risk Of Cancer ◽  
Transit Cell

Abstract Epidermal and intestinal tissues divide throughout life to replace lost surface cells. These renewing tissues have long-lived basal stem cell lineages that divide many times, each division producing one stem cell and one transit cell. The transit cell divides a limited number of times, producing cells that move up from the basal layer and eventually slough off from the surface. If mutation rates are the same in stem and transit divisions, we show that minimal cancer risk is obtained by using the fewest possible stem divisions subject to the constraints imposed by the need to renew the tissue. In this case, stem cells are a necessary risk imposed by the constraints of tissue architecture. Cairns suggested that stem cells may have lower mutation rates than transit cells do. We develop a mathematical model to study the consequences of different stem and transit mutation rates. Our model shows that stem cell mutation rates two or three orders of magnitude less than transit mutation rates may favor relatively more stem divisions and fewer transit divisions, perhaps explaining how renewing tissues allocate cell divisions between long stem and short transit lineages.

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