Biology Reference
In-Depth Information
scoliosis in humans. Observed parallels between the guppy
Curveback
syndrome and human idiopathic scoliosis suggest that the guppy model is
an unexploited resource for the identifi cation of primary etiological factors
involved in curvature. Computed tomography of the guppy has revealed
that vertebral breakage or fusion is not associated with the
Curveback
syndrome. In the guppy, the curves are classifi ed into four types: 1. Nearly
curved, 2. Slightly curved, 3. Moderately curved and 4. Progressed curve.
The curves of greater amplitude begin within 4 dpb (days post birth), while
curves that are initiated after 7 dpb tend not to progress fast in type 2.
Progression of curves is periodic, oscillating between periods of increase or
decrease and relative stability. Selected crossing experiments of the guppies
with different types of curves described above have revealed that the gene
controlling
Curveback
is autosomal recessive. The proportion of affected
Curveback
individuals in the lineage is increased in successive generations
with inbreeding, for example, from 50% of F
2
offspring curvature during
development to 58% in F
3
generation. However, there is a female bias for
curves of high magnitude, i.e., 15% of females have severe (type 5) curvature,
compared to 4% of males. Incidentally, at least one skeletal trait, the size of
the opercle bone is mapped to the sex chromosome of three spine stickleback
(Kimmel et al., 2005).
Led by Morinaga, a team of 18 Japanese scientists undertook a large
scale screening of medaka mutants; in them, the abnormal presence and/or
distribution of germ cells were detected by in
situ
hybridization of
olvas,
the
vasa of medaka (Morinaga et al., 2004). They described 16 mutants caused
by 13 genes, which are classifi ed under four groups. Group 1 consists of
four mutants; three of them are recessive genes that increase the number of
germ cells
.
Of them
seitaka
(
sei
),
kongara
(
kon
) are not viable but
totora
(
tot
)
,
inducing gonadal hypertrophy, is viable. In Group 2,
zanzai
(
zei
) mutant
decreases the number of germ cells. Group 3 includes mostly semi-dominant
or recessive mutants; they are
ekou
(
eko
),
eki
(
eki
)
, shitoku
(
sht
) and
anokuba
(
ano
) and are associated with irregular clustering of germ cells
,
resulting in
testicular hypertrophy, gonadal dysgenesis, tumorigenesis, short body and
twisted trunk, respectively. Group 4 consists of
arara
(
arr
)
, hyou
(
hyo
),
mizore
(
mzr
),
hadare
(
hdr
) and
fubuki
(
fbk
) and are recessive or semi-dominant genes
responsible for fragmented clustering of germ cells
.
Of them,
hyo
alone is
viable. Among all of them, the most interesting one is the
tot
mutant, in
which the hypertrophic gonad is fi lled with immature oocytes. This shows
that oogenesis is arrested prior to the vitellogenic stage, while the germ
cell proliferation continues. The genetic male
tot
mutants possess
Dmy
sequence, indicating that the
tot
phenotype develops independent of the
genetic sex.
The nitroreductase (
Ntr
) gene of
Escherchia coli
encodes an enzyme
that converts prodrugs like metronidiazole (Met) to cytotokins. Hsu et