From ecology point of view: "small" predators.

1) Bacteria, virus, retrovirus.  The more complex the system the harder for predators to get you.  I'm talking about "genetic" predators here.  It is thought (don't remember paper) that DNA evolved because RNA was to "easy" to attack.

2) It is an important step in becoming a longer-lived multicellular organism (see above).  You can't increase life-span if during your life you can't survive the many fast evolving molecular predators.

3) The ability to use and mediate more genes.  More control of differentiation, rate of cells growth, and ability to use different alleles in a more productive manner.

I'm sure some better answers with papers by more well read evolutionary biologist will come.  Above is quick and simple.  Heidi

From ecology point of view: "small" predators.

1) Bacteria, virus, retrovirus.  The more complex the system the harder for predators to get you.  I'm talking about "genetic" predators here.  It is thought (don't remember paper) that DNA evolved because RNA was to "easy" to attack.

2) It is an important step in becoming a longer-lived multicellular organism (see above).  You can't increase life-span if during your life you can't survive the many fast evolving molecular predators.

3) The ability to use and mediate more genes.  More control of differentiation, rate of cells growth, and ability to use different alleles in a more productive manner.

I'm sure some better answers with papers by more well read evolutionary biologist will come.  Above is quick and simple.  Heidi

Hi Heidi

I too believe DNA methylation has contributed to 1 and 3 as you mentioned but I was surprised to see many of the long lived animals are not always much evolved.

I am looking forward to see more suggestions to understand the evolutionary role of DNA methylation.

Thanks 

DNA methylation is a biochemical process where a methyl group is added to the cytosine or adenine DNA nucleotides and it plays a pivotal role for epigenetic gene regulation in development and disease. DNA methylation by the Dnmt family occurs in vertebrates and invertebrates, and is thought to play important roles in gene regulation and genome stability, especially in vertebrates. DNA methylation is highly mutagenic.

In vertebrate genomes, methylation occurs almost exclusively at the cytosines in CpG dinucleotides. Methylated cytosines undergo rapid deamination to become thymines, causing C-to-T transitions (or G-to-A transitions in the complementary strand). However, the “global methylation” patterns of vertebrates and invertebrates are distinctive. Vertebrate genomes exhibit a global DNA methylation pattern (∼80% of the CpGs are methylated) in most cell types and thus are largely depleted of CpG dinucleotides. However, invertebrate such as Drosophila and C. elegans generally lack germ line DNA methylation that is why they possess “mosaic DNA methylation”.

But, Biology is science of exception; the genomes of close outgroup of vertebrates, such as those of invertebrates within the chordate phylum (e.g., urochordate sea squirt and cephalochordate amphixious), and echinoderms (e.g., sea urchin) exhibit a “mosaic” CpG methylation pattern with long methylated regions and equally long unmethylated regions indicating that the transition from mosaic to global methylation pattern have occurred early in vertebrate evolution.

Further readings:

http://www.nature.com/nrg/journal/v9/n6/full/nrg2341.html

http://www.pubfacts.com/detail/21106124/Gradual-transition-from-mosaic-to-global-DNA-methylation-patterns-during-deuterostome-evolution.

http://mbe.oxfordjournals.org/content/25/8/1602.full

http://www.pnas.org/content/111/16/5932.full

All of the above answers look great to me! Additionally, if you're interested in more specific significance of methylation in vertebrates, here's my digestion of a paper explaining 3 theories of the evolutionary significance of genomic imprinting (which uses methylation markers).  

https://ihaveagene.wordpress.com/2014/10/24/why-does-it-matter-if-it-came-from-mom-or-dad-the-evolution-of-genomic-imprinting/

Hi, there are some good papers and reviews from Suzuki and Bird and also from Zemach and Zilberman on this topic. There are some speculations (without experimental backup) that innate immunity (e.g. toll-like receptors that recognize foreign DNA) could have played a role in the transition from mosaic to global methylation in vertebrates.     

Hi Tuncay

Suzuki and Bird have speculated innate immunity has been enhanced by this transition of mosaic to global DNA methylation. Advancements in immunology studies in invertebrates might change this sentence "Invertebrates having 50% unmethylated CpG rich DNA would run the risk of initiating an auto immune response' to are running (hopefully)  and justify the evolutionary significance of global DNA methylation with respect to innate immunity.

The primary function of cytosine methylation seem to be protection of genome against transposon proliferation, satellite repeat expansion as well as from invasive foreign DNA. In invertebrates, this could be the only function of C-methylation. Its strict localisation to repeats potentially explains a mosaic distribution.

Vertebrates adopted other functions of C-methylation in addition to genome surveillance. For example, in humans many developmentally regulated genes are methylated suggesting that it plays an improtant role in differentiation, cell type destiny and gametic imprinting.  It follows that in vertebrates, the C-methylation occurs in both protein coding genes and repeats.This may explain a global character of DNA methylation in these multicellular long living organisms.

We found using the HCoDES assay that we published in Molecular Cell last month that DNA breaks mediated by RAG at the endogenous Igkappa locus are methylated while RAG breaks generated at an artificial chromosomal recombination substrate are not methylated. Furthermore, it appeared that nucleolytic resection of unrepaired breaks  of Jk1 at the kappa locus was inhibited by the first methylated CpG at position 5 of the Jk1 gene segment as evidenced by the accumulation of DNA ends at that position in all genotypes looked at. Furthermore when ends underwent 5' to 3' resection, the strand that was resected was hypo methylated or less clearly, demethylated. This would say that like the function of DNA methylation in bacteria where it inhibits cleavage by restriction enzymes,  one function of methylation in higher eukaryotes is to protect some programmed double strand DNA breaks from nucleolytic resection. 

In invertebrates, there is an interesting link between the extent of gene methylation and the gene's function:  highly expressed "housekeeping" genes are methylated more than genes regulated in response to environmental conditions. See our recent paper in BMC genomics and references therein... 

http://www.biomedcentral.com/1471-2164/15/1109

In bacteria, DNA methylation plays a key role in gene regulation, participating in several mechanisms that generate phenotypic heterogeneity. It is a very clever way to keep different phenotypic subpopulations not involving mutation.

The Roberto Balbotin is a simple but accurately answer

Isn’t it significant in evolution! The supplementation by DNA methylation to cell memory mediated by PcG and TrxG genes to remember the transient signals during the development for a long time?

I think, the extensive marking of DNA by methylation has proven advantageous in long term go and has evolved from a bacterial protection mark to epigenetic memory.

Comments and suggestions are welcome

Dear Venkatesh

Can you elaborate your views. Did you mean genomic expression in organisms which doesn't have DNA methylation is not organised and have less control over it .

El concilio de la "National Evolutionari Synthesis Center sobre el rol de la epigenética heredable en la evolución fenotípica relaciona la herencia epigenética a la plasticidad fenotípica, y ésta como el efecto del entorno sobre el medi ointerno del individuo relacionado con las condiciones de crianza y cuidados maternos en la primeras etapas del desarrollo, y a los mecanismos epigenéticos que subyacen a los efectos fenotípicos persistentes ontogénicos y trnas-generacionales  (herencia epigenética) como el motor de la variación fenotípica heredable que compromete la revisión lamarckiana de la concepción estocástica de la evolución, circunstancia que Jiang admite a medias cuando asevera la interacción de tres factores, los mecanismos de mutación relacionados con la expresión de polimorfirmos, tema que ya han abordado en esta discusión otros investigadores, el tamaño de la población y la selección.