Biology Reference
In-Depth Information
which the cellular or genetic bases underlying metamorphic changes are be-
ing thoroughly investigated, and we highlight some of the many outstanding
questions that remain to be answered.
4.1. Flatfish cranial asymmetry
The most thoroughly studied teleost metamorphic process is undoubtedly
the unique cranial transformation of the flatfish. Although flatfishes are ex-
ceptional in their external morphological asymmetry, the internal organs of
all vertebrates are asymmetric to different degrees. This internal asymmetry
originates during early embryogenesis with the asymmetric expression of ge-
netic cascades that initiate asymmetric expression of the homeobox-
containing transcription factor Pitx2 (
Ryan et al., 1998
). Flatfishes exploit
this internal asymmetry to ultimately achieve external asymmetry at meta-
morphosis (
Hashimoto et al., 2002; Suzuki et al., 2009
). Pitx2 is reexpressed
at metamorphosis in a fundamentally asymmetric portion of the brain, and
this reexpression appears to initiate eye migration (
Suzuki et al., 2009
).
Cellular proliferation in the suborbital tissue of one side of the cranium
may “push” one eye across the dorsal midline (
Bao et al., 2011
). Whether
this proliferation is stimulated by TH directly or whether intermediary sig-
nals are involved remains unknown, but GH and IGF pathways likely serve
as more proximal factors (
Hildahl et al., 2008
). In several flatfish mutants,
cranial asymmetry is decoupled from internal organ asymmetry, suggesting
that the two are regulated by independent mechanisms (
Hashimoto et al.,
2002
). Elucidating the local pattern-forming and morphogenetic cues that
determine the definitive form of the adult craniofacial skeleton, and how
these factors depend on global hormonal effectors, clearly represents an
exciting area for future research.
4.2. Skin
Larval teleosts have a simple integumentary structure, composed primarily
of epidermis; at metamorphosis, the skin becomes increasingly stratified
and complex (
Chang & Hwang, 2011; Hawkes, 1974; Rakers et al.,
2010
). Collagen fibrils are deposited in orthogonal arrays under the
epidermis (
Le Guellec, Morvan-Dubois, & Sire, 2004
) and the acellular
stroma is then invaded by fibroblasts of unknown origin (but potentially
originating from the neural crest;
Matsumoto et al., 1983
). Later, in meta-
morphosis, these fibroblasts initiate scale formation, potentially regulated
