Biology Reference
In-Depth Information
Table 2.1.
Possible paralogies between parts of
human chromosomes 4 and 5 (after Lundin
et al
.,
1993)
4
5
FGFR3
FGFR4
HTR1A
ADRB2
ADRA2C
ADRA1B
DRD5
DRD1
QDPR
DHFR
GABRA2
GABRA1
GABRB1
STATH
SPARC
KIT
PDGFRB
PDGFRA
CSF1R
AREG
C7
EGF
C9
AGA
HEXB
FGF5
FGF2
FGF1
IF
F12
F11
GZMA
KLK3
CSF2
IL2
IL3
IL4
IL5
IL9
CSF1
MLR
GRL
ANX3
ANX5
ANX6
allowed evolutionary experimentation, in that while one gene copy continued to
function as before, the other was freed to acquire mutations, irrespective of
whether they were adaptive or inactivating (Ohta, 1989; 1991). If the newly dupli-
cated gene acquired mutations that modified either the expression pattern of the
encoded gene or the function of the encoded protein in an advantageous way, the
novel allele could have become fixed in the population. Ohno (1970) expressed
this idea rather elegantly:
An escape from the ruthless pressure of natural selection is provided by the
mechanism of gene duplication. By duplication, a redundant copy of a locus is
created. Natural selection often ignores such a redundant copy, and, while
being ignored, it accumulates formerly forbidden mutations and is reborn as a
new gene locus with a hitherto non-existent function. Thus, gene duplication
emerges as the major force of evolution.
In this context, evidence for positive selection (Chapter 7, section 7.1.3) has come
from the observation of accelerated evolution in some genes subsequent to gene
