Biology Reference
In-Depth Information
metamorphic timing and body size are expected to covary and coevolve if
they share a common genetic basis. This prediction holds in the case of
met2.
In the
A. andersoni/A. mexicanum
backcross study described above,
met2
not
only explained significant variation in metamorphic timing but it also
explained significant variation in adult body size (
Voss et al., 2012
). Individ-
uals that delayed metamorphosis significantly increased body length at
300 dpf and weight at 400 dpf, and the effect was approximately equivalent
for sexually dimorphic males and females. Overall, the genetic results
reviewed here show that TH-responsive QTL accounts for variation in
metamorphic timing, expression of metamorphosis versus paedomorphosis,
and adult fitness traits.
9. WHAT GENES MAP TO METAMORPHIC TIMING QTL?
The
A. mexicanum
genome is in early stages of genome sequencing and
thus comparative mapping has been used to more finely resolve the positions
of
met1-3
and identify candidate genes. The most promising candidate that
has been identified is
pou1f1
, a transcription factor associated with combined
pituitary hormone deficiency (CPHD) in humans.
pou1f1
is predicted to
map to the position of
met3
on linkage group (LG) 7
.
CPHD is associated
with deficiencies in the secretion of pituitary hormones that regulate growth
and development, but not hormones associated with reproductive physiol-
ogy. Thus,
pou1f1
is a candidate gene for evolutionary developmental
changes that are independent of reproductive maturation (neoteny), as is
seen in the example of salamander paedomorphosis.
In contrast to
met3
, identifying candidates for
met1 and met2
has
proven more difficult. For example, the 2 cm interval defining the location
of
met1
on LG2 marks a unique synteny disruption in
Ambystoma
and per-
haps other salamanders (
Voss et al., 2011
). This is a bit surprising and unlucky
because the
Ambystoma
genome has undergone relatively few chromosomal
rearrangements relative to other vertebrates and especially amniotes (
Smith
& Voss, 2006
). Genes (e.g.,
rai1
,
shmt1
,
drg2
,
med9
) from the Smith-Magenis
disease syndrome region in the human genome flank one side of
met1
, while
several genes associated with neural development and function (e.g.,
setd2
,
ngfr
,
ccm2
) flank the other side. In no other vertebrate genome are these
groups of flanking markers observed in synteny. Recently, we used micro-
array analysis to identify genes that are expressed differently during larval de-
velopment as a function of
met1
genotype (Robert Page and Randal Voss,
unpublished data). We reasoned that
this combined genetic-genomic
