Mechanism of evolution by genetic assimilation

Abstract

Conrad H. Waddington discovered the phenomenon of genetic assimilation through a series of experiments on fruit flies. In those experiments, artificially exerted environmental stress induced plastic phenotypic changes in the fruit flies, but after some generations, the same phenotypic variant started to appear without the environmental stress. Both the initial state (where the phenotypic changes were environmentally induced and plastic) and the final state (where the phenotypic changes were genetically fixed and constitutive) are experimental facts. However, it remains unclear how the environmentally induced phenotypic change in the first generation becomes genetically fixed in the central process of genetic assimilation itself. We have argued that the key to understanding the mechanism of genetic assimilation lies in epigenetics, and proposed the "cooperative model" in which the evolutionary process depends on both genetic and epigenetic factors. Evolutionary simulations based on the cooperative model reproduced the process of genetic assimilation. Detailed analysis of the trajectories has revealed genetic assimilation is a process in which epigenetically induced phenotypic changes are incrementally and statistically replaced with multiple minor genetic mutations through natural selection. In this scenario, epigenetic and genetic changes may be considered as mutually independent but equivalent in terms of their effects on phenotypic changes. This finding rejects the common (and confused) hypothesis that epigenetically induced phenotypic changes depend on genetic mutations. Furthermore, we argue that transgenerational epigenetic inheritance is not required for evolution by genetic assimilation.

Bridging Tumorigenesis and Therapy Resistance With a Non-Darwinian and Non-Lamarckian Mechanism of Adaptive Evolution

“…Alternatively, epigenetic configurations that are advantageous in the therapeutic environment may be pre-existing and undergo positive selection (30,31). Moreover, while resistance can be coupled with purely epigenetic or purely genetic changes, it is also possible that initially non-genetic changes become genetically hardwired/assimilated over time, i.e., an environmentally induced phenotype is made constitutive (12,32,33). In sum, cancer populations can achieve drug resistance through genetic and/or non-genetic means and via a mix of neo-Darwinian and quasi-Lamarckian mechanisms of adaptive evolution (a fully Lamarckian scheme of adaptation would entail, inter alia, that environmental factors cause directed adaptive changes).…”

Long-Term m5C Methylome Dynamics Parallel Phenotypic Adaptation in the CyanobacteriumTrichodesmium

“…2017 ). Epigenetic regulation can mediate phenotypic plasticity in response to environmental change ( West-Eberhard 2005 ; Nishikawa and Kinjo 2018 ). Phenotypic plasticity can be defined as a short-term change in phenotype in response to a perturbation without a change in the underlying genotype.…”

“…2016 ; Kronholm et al. 2017 ; Nishikawa and Kinjo 2018 ). This is especially important because the two processes can be linked, where epigenetics can “lead the way” for genetic adaptation to occur.…”

Heterogeneity of primordial germ cells

“…It has been dubbed an "evolutionary capacitor" because its absence in a number of organisms leads to enhanced phenotypic variability that is believed to arise from cryptic protein variants that are normally degraded or chaperoned by Hsp90 (Rutherford & Lindquist, 1998;Specchia et al, 2010). Most cell types express Hsp90b and elevate expression in stressful conditions, but an A isoform is exclusive to germ cells (Nishikawa & Kinjo, 2018). Hsp90a was further linked to germ cell development through its interaction with the germ plasm component and piRNA biogenesis factor Piwi (Gangaraju et al, 2010).…”