Impact of NoncodingDNAon Phenotype Evolution

Abstract

A major discovery in science was the central dogma : that the digital code of DNA was read and translated by RNA into proteins. The information carried by DNA is thus the genotype, which constitutes the phenotype. While the genotype–phenotype discussion primarily concerns the role of ‘real’ protein‐coding genes, the impact of non‐protein‐coding elements like transposons on the phenotype has been less recognised. Such noncoding elements constitute however a major share of most genomes, and genome size per se may display a tremendous variability even between closely related organisms. Whether noncoding elements are parasitic ‘junk DNA’ or are transcribed and thus affect the phenotype is a matter of heated debate. Whether seen as junk or not, noncoding DNA strongly boosts the share genome size, thereby affecting a range of fitness‐related phenotypic traits like mutation rate, genomic flexibility, cell size, body size, morphology, growth rate, behaviour, life cycle and potentially also speciation. Key Concepts The central dogma postulates that the blueprint of life is coded in the genes, which is read by RNA to produce protein. Thus the genotype constitutes the phenotype. The genotype (the sum of all DNA) is in most organisms made up by non‐protein‐coding DNA, often dominated by virus‐like transposable elements, and whether this is ‘junk’ or ‘parasitic’ DNA of which has a clear function is a heated debate. The C‐value paradox points to the striking variability in genome size even between related organisms, which do not reflect organism complexity. Even if the noncoding DNA is seen as ‘junk’, it has however wide implications for a range of phenotypic traits such as cell size, growth rate, metabolism and life history and is an important yet often neglected part of the genotype–phenotype link. The genome is far more flexible and dynamic than often recognised and is still full of surprises.