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Mutational hazard hypothesis

The mutational hazard hypothesis is a non-adaptive theory for increased complexity in genomes. The basis of mutational hazard hypothesis is that each mutation for non-coding DNA imposes a fitness cost. Variation in complexity can be described by 2N_eu, where N_e is effective population size and u is mutation rate.

In this hypothesis, selection against non-coding DNA can be reduced in three ways: random genetic drift, recombination rate, and mutation rate. As complexity increases from prokaryotes to multicellular eukaryotes, effective population size decreases, subsequently increasing the strength of random genetic drift. This, along with low recombination rate and high mutation rate, allows non-coding DNA to proliferate without being removed by purifying selection.

Accumulation of non-coding DNA in larger genomes can be seen when comparing genome size and genome content across eukaryotic taxa. There is a positive correlation between genome size and non-coding-DNA-genome-content with each group staying within some variation. When comparing variation in complexity in organelles, effective population size is replaced with genetic effective population size (N_g). If looking at silent-site nucleotide diversity, then larger genomes are expected to have less diversity than more compact ones. In plant and animal mitochondria, differences in mutation rate account for the opposite directions in complexity, with plant mitochondria being more complex and animal mitochondria more streamlined.

The mutational hazard hypothesis has been used to at least partially explain expanded genomes in some species. For example, when comparing Volvox cateri to a close relative with a compact genome, Chlamydomonas reinhardtii, the former had less silent-site diversity than the latter in nuclear, mitochondrial, and plastid genomes. However when comparing the plastid genome of Volvox cateri to Volvox africanus, a species in the same genus but with half the plastid genome size, there was high mutation rates in intergenic regions. In Arabiopsis thaliana, the hypothesis was used as a possible explanation for intron loss and compact genome size. When compared to Arabidopsis lyrata, researchers found a higher mutation rate overall and in lost introns (an intron that is no longer transcribed or spliced) compared to conserved introns.

There are expanded genomes in other species that could not be explained by the mutational hazard hypothesis. For example, the expanded mitochondrial genomes of Silene noctiflora and Silene conica have high mutation rates, lower intron lengths, and more non-coding DNA elements compared to others in the same genus, but there was no evidence for long-term low effective population size. The mitochondrial genomes of Citrullus lanatus and Curcurbita pepo differ in several ways. Citrullus lanatus is smaller, has more introns and duplications, while Curcurbita pepo is larger with more chloroplast and short repeated sequences. If RNA editing sites and mutation rate lined up, then Curcurbita pepo would have a lower mutation rate and more RNA editing sites. However the mutation rate is four times higher than Citrullus lanatus and they have a similar number of RNA editing sites. There was also an attempt to use the hypothesis to explain large nuclear genomes of salamanders, but researchers found opposite results than expected, including lower long-term strength of genetic drift.