Each haplogroup has a sequence of specific mutations that identify it (Table 1).
Consider for example de novo genes (e.g., [ 9- 13])—genes that presumably have arisen "out of thin air" by a sequence of random mutations that came together into a new functioning gene, including signals for transcription and translation and even alternative splicing [ 11].
In terms of our model, this suggests a m→m+/a→A sequence of mutations, in which the novel Sxl allele (A allele at the R locus) was capable of up-regulating an ancestral m+ allele of tra (D locus).
Tracing along the line of descent (shown in red) gives a specific sequence of mutations; we can use these to reconstruct the corresponding path through sequence space (a directed graph through the space of all possible protein sequences), as shown at the bottom of the figure.
It is preferable for the fitness of solutions to change smoothly as they evolve, with improvements in fitness tied directly to particular sections of the chromosome, rather than relying on a very specific sequence of mutations to occasionally create a large improvement in fitness.
For a mutation rate μ, the probability that a sequence of length l acquires k mutations upon replication follows a Poisson distribution of average μl, (4) The probability of incorporating no mutations is thus P 0) = e- μl, which for μl ≪ 1 reduces to P 0) = 1 - μl.
According to Griffiths and Tavaré (1995), the set of nonrecombining haplotypes carrying these mutations is identical to a rooted gene tree, and the sequence of mutations corresponds to the path from the haplotype to the common ancestor [the root of the gene tree, see Griffiths and Tavaré (1995) for a detailed discussion].
Here we present a sequence analysis of mutation events and a description of the structure of repeated regions in the hypervariable, pentanucleotide microsatellite locus HrU10 in barn swallows (Hirundo rustica) and tree swallows (Tachycineta bicolor).
Sequencing their genomes and monitoring polarization reveals a common evolutionary trajectory, with a fixed sequence of adaptive mutations, each improving cell polarization by inactivating proteins.
