Epigenetics and Evolution: Transposons and the Stochastic Epigenetic Modification Model

Sergio Branciamore; Andrei S. Rodin; Grigoriy Gogoshin; Arthur D. Riggs; Sergio Branciamore; Andrei S. Rodin; Grigoriy Gogoshin; Arthur D. Riggs

doi:10.3934/genet.2015.2.148

AIMS Genetics

2015, Volume 2, Issue 2: 148-162. doi: 10.3934/genet.2015.2.148

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Epigenetics and Evolution: Transposons and the Stochastic Epigenetic Modification Model

Department of Diabetes and Metabolic Diseases Research, Beckman Research Institute of City of Hope, 1500 East Duarte Road, Duarte, CA 91010, USA
Sergio Branciamore, Andrei S. Rodin and Grigoriy Gogoshin contributed equally to this work.

Received: 08 January 2015 Accepted: 06 April 2015 Published: 18 April 2015

In addition to genetic variation, epigenetic variation and transposons can greatly affect the evolutionary fitnesses landscape and gene expression. Previously we proposed a mathematical treatment of a general epigenetic variation model that we called Stochastic Epigenetic Modification (SEM) model. In this study we follow up with a special case, the Transposon Silencing Model (TSM), with, once again, emphasis on quantitative treatment. We have investigated the evolutionary effects of epigenetic changes due to transposon (T) insertions; in particular, we have considered a typical gene locus A and postulated that (i) the expression level of gene A depends on the epigenetic state (active or inactive) of a cis- located transposon element T, (ii) stochastic variability in the epigenetic silencing of T occurs only in a short window of opportunity during development, (iii) the epigenetic state is then stable during further development, and (iv) the epigenetic memory is fully reset at each generation. We develop the model using two complementary approaches: a standard analytical population genetics framework (di usion equations) and Monte-Carlo simulations. Both approaches led to similar estimates for the probability of fixation and time of fixation of locus TA with initial frequency P in a randomly mating diploid population of effective size N_e. We have ascertained the e ect that ρ, the probability of transposon Modification during the developmental window, has on the population (species). One of our principal conclusions is that as ρ increases, the pattern of fixation of the combined TA locus goes from "neutral" to "dominant" to "over-dominant". We observe that, under realistic values of ρ, epigenetic Modifications can provide an e cient mechanism for more rapid fixation of transposons and cis-located gene alleles. The results obtained suggest that epigenetic silencing, even if strictly transient (being reset at each generation), can still have signi cant macro-evolutionary effects. Importantly, this conclusion also holds for the static fitness landscape. To the best of our knowledge, no previous analytical modeling has treated stochastic epigenetic changes during a window of opportunity.
- DNA methylation,
- mathematical modeling,
- computational biology,
- developmental biology,
- molecular evolution
Citation: Sergio Branciamore, Andrei S. Rodin, Grigoriy Gogoshin, Arthur D. Riggs. Epigenetics and Evolution: Transposons and the Stochastic Epigenetic Modification Model[J]. AIMS Genetics, 2015, 2(2): 148-162. doi: 10.3934/genet.2015.2.148

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Abstract

In addition to genetic variation, epigenetic variation and transposons can greatly affect the evolutionary fitnesses landscape and gene expression. Previously we proposed a mathematical treatment of a general epigenetic variation model that we called Stochastic Epigenetic Modification (SEM) model. In this study we follow up with a special case, the Transposon Silencing Model (TSM), with, once again, emphasis on quantitative treatment. We have investigated the evolutionary effects of epigenetic changes due to transposon (T) insertions; in particular, we have considered a typical gene locus A and postulated that (i) the expression level of gene A depends on the epigenetic state (active or inactive) of a cis- located transposon element T, (ii) stochastic variability in the epigenetic silencing of T occurs only in a short window of opportunity during development, (iii) the epigenetic state is then stable during further development, and (iv) the epigenetic memory is fully reset at each generation. We develop the model using two complementary approaches: a standard analytical population genetics framework (di usion equations) and Monte-Carlo simulations. Both approaches led to similar estimates for the probability of fixation and time of fixation of locus TA with initial frequency P in a randomly mating diploid population of effective size N_e. We have ascertained the e ect that ρ, the probability of transposon Modification during the developmental window, has on the population (species). One of our principal conclusions is that as ρ increases, the pattern of fixation of the combined TA locus goes from "neutral" to "dominant" to "over-dominant". We observe that, under realistic values of ρ, epigenetic Modifications can provide an e cient mechanism for more rapid fixation of transposons and cis-located gene alleles. The results obtained suggest that epigenetic silencing, even if strictly transient (being reset at each generation), can still have signi cant macro-evolutionary effects. Importantly, this conclusion also holds for the static fitness landscape. To the best of our knowledge, no previous analytical modeling has treated stochastic epigenetic changes during a window of opportunity.

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