The actions of in ovo cortisol on egg fertility, embryo development and the expression of growth‐related genes in rainbow trout embryos, and the growth performance of juveniles

Abstract

Rainbow trout (Oncorhynchus mykiss) oocytes were incubated for 3 hr in ovarian fluid alone (CC), or cortisol-enriched ovarian fluid [100 or 1,000 ng ml(-1) (CL and CH, respectively)], after which they were fertilized; the growth and development of the embryos reared from these oocytes was monitored until first feed, and the juveniles were monitored for 9 months. The hatching rates of the CH group were significantly reduced, but the overall survival as measured at 40-week post-fertilization was similar in the three treatment groups. In addition, significant apparently biphasic changes relative to the CC group were found in the expression of some key growth-related genes in the CL and CH treatment groups, particularly IGF-1, IGF-2, GH1, GH2, GH receptors, and thyroid hormone receptors (TRα and TRβ). Moreover, the juveniles of the CL (but not the CH treatment group) exhibited enhanced growth; the enhanced growth could not be explained on the basis of increased feed conversion efficiency or changes in serum GH levels at the juvenile stage. Additionally, relative growth rates from the three treatment groups were similar, suggesting that the biphasic growth-enhancing effects of cortisol occurred very early in embryogenesis.

Maternal Experience with Predation Risk Influences Genome-Wide Embryonic Gene Expression in Threespined Sticklebacks (Gasterosteus aculeatus)

“…In general, maternal exposure to predation risk had an activating effect on offspring genome-wide expression and affected biological pathways involved in energy homeostasis, proliferation of cells, production of neurites and blood cells, differentiation of sensory neurons, and immunity. Many of these results are consistent with previous findings in sticklebacks and other animals that associated maternal stress with increased offspring growth [22], [43] and metabolism [33], altered immune function [59] and behavior [20], [33], [36]. Our data suggest that when mothers are exposed to a stressor, a shift occurs at the molecular level in offspring resulting in a divergence in the developmental program.…”

“…Glucocorticoids can affect immunity [43], [59] and as expected, many genes involved in the immune response were differentially expressed in maternally-stressed embryos. Four genes encoding complement component 3 (C3) were significantly downregulated in maternally-stressed embryos, but a different two C3 genes were upregulated.…”

“…Third, previous studies have shown that exposing fish embryos to elevated cortisol alters the expression of genes encoding insulin-like growth factor, growth hormone, thyroid hormone receptors, and growth hormone receptors [43]. Since stickleback mothers produce eggs with elevated cortisol after exposure to a predator [33] we predicted that genes that are activated or repressed by cortisol or synthetic glucocorticoids would be differentially expressed between treatments.…”

Maternal Thyroid and Glucocorticoid Hormone Interactions in Larval Fish Development, and Their Applications in Aquaculture

“…Cortisol suppression of IGF-1 expression seems to be conserved in teleosts, but in hepatocytes of coho salmon (Pierce et al, 2010) and tilapia (Pierce et al, 2011) cortisol was shown to up-regulate IGF-2 mRNA levels, either directly or via enhanced Growth Hormone (GH) response. In rainbow trout embryos reared from cortisolenriched oocytes, however, IGF-1 expression was significantly enhanced from the zygote to 21-days post-fertilization (dpf) embryos and IGF-2 was enhanced in the 21-dpf embryos (Li et al, 2010). These results suggest that the regulation of IGF expression by cortisol may be different in fish embryos from that in adults, and cortisol may act via IGF-1 and/or IGF-2 signals to regulate embryogenesis.…”

Genes Contributing to Genetic Variation of Muscling in Sheep

“…Over-expression of LAP in mouse results in muscle mass enhancement. This is due to the ability of LAP to bind MSTN and inhibit its signaling activity (Li et al, 2010). Several circulating MSTN binding proteins [follistatin, decorin, small glutamine rich tetratricopeptide repeat (SGT), titan cap, Grb2-associating protein (GASP), follistatin related gene protein (FLRG)] have been identified in mouse.…”