Biology Reference
In-Depth Information
Table 8.3.
Mechanism-based evolution of the repeat segments of involucrin in mammals
(from Green and Djian, 1992)
Mechanism
Organism in which mechanism
operates
Shortening or lengthening of pre-existing Site P of prosimians, tarsioids and non-primate
repeats by site-specific deletion or insertion. mammals. Not operative in anthropoid apes.
Change in consensus nucleotide at certain
Site P of prosimians, tarsioids and non-primate
positions resulting from mutation in one
mammals. Not operative in anthropoid apes.
repeat followed by correction of
neighboring repeats (probably by gene
conversion). Many of the corrections are
silent.
Addition of shorter repeats as incomplete
Site P of tarsioids. Not operative in anthropoid
copies of older ones.
apes.
Generation of a new duplication site (M) by
Tarsioids and anthropoid apes. Aborted in
vectorial addition of repeats at a controlled
tarsioids. Not operative in prosimians and non-
hotspot moving in a 3
→
5 direction. The
primate mammals.
site of addition differs in different human
populations and is therefore under genetic
control.
hairlessness (Green and Djian, 1992). The P segment of repeats could conceivably
have conferred some selective advantage during the early stages of mammalian
and primate evolution as might the M segment when it emerged. At a biochemi-
cal level, natural selection might have favored the retention of repeat-bearing seg-
ments in involucrin so as to provide a substrate for transglutaminase. Once the M
segment had been generated, the repeats at site P could then have been deleted
without selective disadvantage. However, there is a very considerable degree of
latitude between different species in terms of what constitutes an effective transg-
lutaminase substrate. In a comparison of the involucrins of 19 mammalian
species, only 3.1% of amino acid residues were uniformly conserved (Djian
et al
.,
1993). Thus, on balance, neither the very high rate of evolutionary change nor
the observed patterns of mutational change in the involucrin gene provide
convincing evidence for natural selection being the major motive force behind
involucrin evolution in higher primates. Indeed, it is unlikely that natural selec-
tion could account on its own for either the highly variable pattern of repeat addi-
tion or the numbers of repeats added.
Natural selection and neutral mutation/genetic drift are both processes that
govern how mutations, once they have arisen, spread through a population with
the possibility of eventually becoming fixed. By contrast, the evolution of involu-
crin appears to be primarily mechanism-based, being dominated by endogenously
controlled and spatially targeted mechanisms of mutagenesis. Such mechanisms
are likely to be the major factor responsible for the
directed evolution
of involucrin,
directed in the sense that the mechanisms promote change in a specific direction
(i.e. increases in repeat number or gene conversion between homologous repeats;
see
Table 8.3
) without the necessary assistance of natural selection.
