DNA Replication Timing, Genome Stability and Non-adaptive Radiation

TL;DR

This paper explores how DNA replication timing and genome stability influence species diversity and karyotype variation in mammals, linking molecular processes to evolutionary patterns.

Contribution

It investigates the role of DNA replication timing and repair mechanisms in shaping genome diversity and speciation in mammals.

Findings

Mutation and substitution rates increase with DNA replication timing.

Genome stability factors correlate with species richness.

DNA replication timing impacts karyotype diversity.

Abstract

A correlation between karyotype diversity and species richness was first observed in mammals in 1980, and subsequently confirmed after controlling for phylogenetic signal. The correlation was attributed to submicroscopic factors, presumably operating at the level of the genome. At the same time, an unexpected association between mutation rates and substitution rates has been observed in all eukaryotes so far examined. One hypothesis to explain the latter observation proposed that neutral mutation (dS) and non-neutral (dN) substitution rates in gene codons co-vary according to genomic position, or location in the genome. Later, it was found that mutation and substitution rates in eukaryotes increase with DNA replication timing during the Synthetic phase, or S phase, of the cell cycle. In 1991, Motoo Kimura proposed a molecular theory of non-adaptive radiation (NAR). Accordingly, genetic drift plays a significant role in speciation, albeit in parallel to and in conjunction with natural selection. The following will examine the contribution of DNA replication timing and DNA repair factors to the relationship between species richness and karyotype diversity, and by extension, to the large variation in species richness across the mammalian Tree of Life.