Gi. Bell et J. Jurka, THE LENGTH DISTRIBUTION OF PERFECT DIMER REPETITIVE DNA IS CONSISTENTWITH ITS EVOLUTION BY AN UNBIASED SINGLE-STEP MUTATION PROCESS, Journal of molecular evolution, 44(4), 1997, pp. 414-421
We have examined the length distribution of perfect dimer repeats, whe
re perfect means uninterrupted by any other base, using data from GenB
ank on primates and rodents, Virtually no lengths greater than 30 repe
ats are found, except for rodent AG repeats, which extend to 35, Compa
rable numbers of long AC and AG repeats suggest that they have not bee
n selected for special functions or DNA structures. We have compared t
he data with predictions of two models: (1) a Bemoulli Model in which
bases are assumed equally likely and distributed at random and (2) an
Unbiased Random Walk. Model (URWM) in which repeats are permitted to c
hange length by plus or minus one unit, with equal probabilities, and
in which base substitutions are allowed to destroy long perfect repeat
s, producing two shorter perfect repeats. The source of repeats is ass
umed to be from single base substitutions from neighboring sequences,
i,e., those differing from the perfect repeat by a single base. Mutati
on rates either independent of repeal length or proportional to length
were considered. An upper limit to the lengths L approximate to 30 is
assumed and isolated dimers are assumed unable to expand, so that the
re are absorbing barriers to the random walk at lengths 1 and L + 1, a
nd a steady state of lengths is reached. With these assumptions and es
timated values for the rates of length mutation and base substitution.
reasonable agreement is found with the data for lengths > 5 repeats.
Shorter repeats, of lengths less than or equal to 3 are in general agr
eement with the Bemoulli Model. By reducing the rate of length mutatio
ns for n less than or equal to 5, it is possible to obtain reasonable
agreement with the full range of data, For these reduced rates, the ti
mes between length mutations become comparable to those suggested for
a bottleneck in the evolution of Homo sapiens, which may be tile reaso
n for low heterozygosity of short repeats.