Epigenetics Decouples Mutational from Environmental Robustness. Did It Also Facilitate Multicellularity? (original) (raw)
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Epigenetic Feedback Regulation Accelerates Adaptation and Evolution
PLoS ONE, 2013
A simple cell model consisting of a gene regulatory network with epigenetic feedback regulation is studied to evaluate the effect of epigenetic dynamics on adaptation and evolution. We find that, the type of epigenetic dynamics considered enables a cell to adapt to unfamiliar environmental changes, for which no regulatory program has been prepared, through noise-driven selection of a cellular state with a high growth rate. Furthermore, we demonstrate that the inclusion of epigenetic regulation promotes evolutionary development of a regulatory network that can respond to environmental changes in a fast and precise manner. These results strongly suggest that epigenetic feedback regulation in gene expression dynamics provides a significant increase in fitness by engendering an increase in cellular plasticity during adaptation and evolution.
On the developmental self-regulatory dynamics and evolution of individuated multicellular organisms
On the developmental self-regulatory dynamics and evolution of individuated multicellular organisms
Changes in gene expression are thought to regulate the cell differentiation process intrinsically through complex epigenetic mechanisms. In fundamental terms, however, this assumed regulation refers only to the intricate propagation of changes in gene expression or else leads to non-explanatory regresses. The developmental self-regulatory dynamics and evolution of individuated multicellular organisms also lack a unified and falsifiable description. To fill this gap, I computationally analyzed publicly available high-throughput data of histone H3 post-translational modifications and mRNA abundance for different Homo sapiens, Mus musculus, and Drosophila melanogaster cell-type/developmental-period samples. My analysis of genomic regions adjacent to transcription start sites generated a profile from pairwise partial correlations between histone modifications controlling for the respective mRNA levels for each cell-type/developmental-period dataset. I found that these profiles, while explicitly uncorrelated with the respective transcriptional "identities" by construction, associate strongly with cell differentiation states. This association is not expected if cell differentiation is, in effect, regulated by epigenetic mechanisms. Based on these results, I propose a general, falsifiable theory of individuated multicellularity, which relies on the synergistic coupling across the extracellular space of two explicitly uncorrelated "self-organizing" systems constraining histone modification states at the same sites. This theory describes how the simplest multicellular individual—understood as an intrinsic, higher-order constraint—emerges from proliferating undifferentiated cells, and could explain the intrinsic regulation of gene transcriptional changes for cell differentiation and the evolution of individuated multicellular organisms.
2015
Multicellular organisms have evolved multiple times throughout the history of life on Earth. The most recent transition to multicellularity occurred about 200 MYA within the volvocine algae, with phenotypes ranging from unicellular, undifferentiated multicellular and differentiated multicellular all with sequenced genomes. Interestingly, while the genomes of these organisms are very similar showing only a small increase in the number of genes as morphological complexity increases, the number of histones genes is reduced as morphological complexity increases. Compared to Chlamydomonas reinhardtii, unicellular, and Gonium pectorale, colonial multicellular, which have 125 and 133 histones respectively, Volvox carteri, differentiated multicellular, only has 54 histone genes. This reduction in histones is unexpected since increasing in complexity and increasing cellular differentiation should require more histones to regulate the differential expression between tissues. One possible expl...
Version 10 Epigenetic catalysis in an evolutionary context
2009
Recent work by Ciliberti et al. nds the spinglass model of regulatory gene networks adapted from neural network stud- ies to have a single giant connected component in a metanet- work space of interaction matrices, permitting only gradual evolutionary transition, in conict with empirical studies of development in sea urchin species that found evidence for punctuated equilibrium evolutionary transition. Shifting
Epigenetic control: slow and global, nimble and local
Genes & Development, 2008
The regulation of gene expression involves multiple levels of control, from those that are inheritable to those that are highly responsive to environmental changes. In this issue of Genes & Development, Dong and colleagues (pp. 1159-1173) demonstrate that the dynamically controlled immune response transcription factor NF-B may, in fact, have a role in regulating heterochromatin and gene expression at large distances from its actual target sequences and genes.
Genetic and Epigenetic Regulation Schemes: Need for an Alternative Paradigm
Molecular Genetics and Metabolism, 2000
Self-organization of living cells results from the tangle of positive and negative feedback developed to ensure their homeostasis and/or their differentiation. There are three major means cellular regulation operates: the genetic, the epigenetic, and the metabolic ones. The regulation type in each of them has been overviewed. Further examination of relations between complexity and developmental stability points out sui generis properties of feedback loops, which are redundancy and pleiotropy. Prototypical schemes for positive and negative regulation with redundant and pleiotropic (including multifunctional) proteins are presented. They stress a theoretical shift from the analytical to the systemic framework. The systemic paradigm appears to be of increasing interest and importance in the study of concepts for the representation of genetic and epigenetic regulations.
Journal of Theoretical Biology, 2015
An enduring puzzle in evolutionary biology is to understand how individuals and populations adapt to fluctuating environments. Here we present an integro-differential model of adaptive dynamics in a phenotype-structured population whose fitness landscape evolves in time due to periodic environmental oscillations. The analytical tractability of our model allows for a systematic investigation of the relative contributions of heritable variations in gene expression, environmental changes and natural selection as drivers of phenotypic adaptation. We show that environmental fluctuations can induce the population to enter an unstable and fluctuation-driven epigenetic state. We demonstrate that this can trigger the emergence of oscillations in the size of the population, and we establish a full characterisation of such oscillations. Moreover, the results of our analyses provide a formal basis for the claim that higher rates of epimutations can bring about higher levels of intrapopulation heterogeneity, whilst intense selection pressures can deplete variation in the phenotypic pool of asexual populations. Finally, our work illustrates how the dynamics of the population size is led by a strong synergism between the rate of phenotypic variation and the frequency of environmental oscillations, and identifies possible ecological conditions that promote the maximisation of the population size in fluctuating environments.