Developmental ontogeny of prolactin and prolactin receptor
in the sea bream (Sparus aurata)
C.R.A. Santos,
a
J.E.B. Cavaco,
a
P.M. Ingleton,
b
and D.M. Power
a,
*
a
Universidade do Algarve, CCMAR, Centre of Marine Sciences, Campus de Gambelas, Faro 8000-810, Portugal
b
Academic Unit of Endocrinology, Division of Genomic Medicine, G Floor, Medical School, Sheffield S10 2RX, UK
Accepted 22 January 2003
Abstract
The expression of PRL and its receptor (PRLR) were characterised during sea bream embryonic and larval development, by
semi-quantitative and quantitative RT-PCR, respectively, until 46 days post-hatch (DPH). Immunocytochemistry with antisera
specific for sea bream PRLR was carried out with larval sections from hatching up to 46 DPH. A single transcript of PRL (1.35 Kb)
and PRLR (2.8 Kb) identical to the transcripts previously characterised in adult tissue, are present in sea bream embryos and larvae.
PRL expression is first detectable at neurula and in all samples collected thereafter. The lowest levels of PRL mRNA are detected in
sea bream embryos up until neurula when expression starts to increase. The maximal levels of PRL expression were detected at 24
DPH. PRLR transcripts first appear at 12 h post-fertilisation (0:002 qmol=lg total larvae RNA) (blastula) and increase significantly
during gastrulation (0:245 qmol=lg total larvae RNA) reaching a maximum at 2 DPH (0:281 qmol=lg total larvae RNA). After
hatching a significant reduction in PRLR expression is observed which reaches a minimum at 4 DPH (0:103 qmol=lg total larvae
RNA), gradually increasing thereafter. Immunocytochemistry revealed the presence of PRLR in early post-hatching stages of larvae
in tissues derived from all three germ layers.
Ó 2003 Elsevier Science (USA). All rights reserved.
1. Introduction
The role of prolactin (PRL) in embryogenesis has
received increased attention over the past few years. In
the earliest stages of embryonic development, growth-
promoting molecules must be provided by the maternal
system via the egg. These molecules may be either hor-
mones or growth factors, or other molecules, which in-
teract with these. Prolactin has been implicated in the
control of embryonic growth and some studies suggest
that embryos may be able to utilise PRL of maternal
origin during organogenesis (Karabulut and Pratten,
1998). Moreover, it appears that in rats, PRL influences
the actions of insulin-like growth factors (IGFs) and
their receptors in order to mediate embryo growth
(Karabulut et al., 1999). In early developmental stages
of humans and rats intense PRL receptor (PRLR) im-
munoreactivity has been observed in tissues derived
from embryonic mesoderm, including the periadrenal
and perinephric mesenchyme, pulmonary and duodenal
mesenchyme, cardiac and skeletal myocytes, as well as
the mesenchymal precartilage and maturing chondro-
cytes of the craniofacial and long bones, and the verte-
brae and ribs (Freemark et al., 1997). These
observations suggest that PRL is likely to play a role in
tissue differentiation and organ development in early
gestation (Freemark et al., 1997). Expression of PRLR
mRNA and protein are also widespread throughout the
foetus, with especially high levels in developing bone
and cartilage, thymus, pituitary, tongue and skeletal
muscle, and certain regions of the brain (Tzeng and
Linzer, 1997) reinforcing the idea that PRL may be es-
sential for embryo development. Moreover, PRLR
knockout mice show compromised development of
skeletal structures (Clement-Lacroix et al., 1999).
A PRLR of sea bream has recently been cloned (Santos
et al., 2001) which in common with the receptors of Nile
tilapia (Oreochromis niloticus) (Sandra et al., 1995), mos-
sambican tilapia (Oreochromis mossambicus) (Shiraishi
General and Comparative Endocrinology 132 (2003) 304–314
www.elsevier.com/locate/ygcen
GENERAL AND COMPARATIVE
ENDOCRINOLOGY
*
Corresponding author. Fax: +351-89-818419.
E-mail address: dpower@ualg.pt (D.M. Power).
0016-6480/03/$ - see front matter Ó 2003 Elsevier Science (USA). All rights reserved.
doi:10.1016/S0016-6480(03)00083-2