Fig. 6

A model of satDNA evolution. We consider that evolutionary events are rather different at intra- and intergenomic levels. At intragenomic level, tandem duplication gives birth to a new tandem repeat and its reiteration yields many copies of identical noncoding sequences (satDNA amplification). The newly amplified satDNA displays RLs sharply leptokurtic (a). As time goes by, point mutation increases divergence among the amplified sequences and the curve progressively is flattened (b–e) and DIVPEAK (i.e., the divergence value showing the higher abundance) increases (i.e., the peak moves to the right in the a–e graphs). At any moment of this first amplification-degeneration cycle, another sequence undergoes amplification and begins a new cycle. This sets the satDNA family farther from degeneration and extinction because its average divergence decreases and now predominates a newly amplified subfamily with leptokurtic RL (we represent here three successive cycles of amplification; note that the differences in size among cycles are to facilitate drawing and have nothing to do with amplification level). In parallel, an intragenomic spread of the satDNA can occur at higher or lower extent (brown stars). A conceivable exit of these cycles is satDNA degeneration, when homology with the original sequence is lost. At intergenomic level, individual reproduction will mark the destiny of the different satDNA sequences in populations. When reproduction is differential, albeit random (drift) or non-random (selection), some sequences may become prevalent above others. At this respect, the mutational-hazard hypothesis is applicable to explain the limits to purifying selection in some species showing extremely high abundance of satDNA. Finally, we cannot rule out that, in some case, transmission drive could help satDNA to prosper and, even that positive selection may recruit satDNA for important functions, such as telomeric or centromeric functions