Glucocorticoid receptor activation following elevated oocyte cortisol content is associated with zygote activation, early embryo cell division, and IGF system gene responses in rainbow trout.
Increased in ovo cortisol content of rainbow trout oocytes from ~3·5 to ~5·0 ng.oocyte(-1) before fertilization enhances the growth of embryos and juveniles and changes the long-term expression pattern of IGF-related genes. This study used embryos reared from oocytes enriched with cortisol and the glucocorticoid receptor (GR) antagonist, RU486, to determine whether the growth-promoting actions of cortisol involve GR protein activation and modulation of gr expression. Whole-mount in situ immunohistofluorescence studies of zygotes showed that enhanced oocyte cortisol increased the immunofluorescent GR signal and activated the relocation of GR from a general distribution throughout the cytoplasm to an accumulation in the peri-nuclear cytoplasm. In ovo cortisol treatment increased the number of embryonic cells within 48-h post-fertilization, and RU486 partially suppressed this cortisol stimulation of cell duplication. In addition, there was complex interplay between the expression of gr and igf system-related genes spatiotemporally in the different treatment groups, suggesting a role for GR in the regulation of the expression of development. Taken together, these findings indicate an essential role for GR in the regulation of epigenomic events in very early embryos that promoted the long-term growth effects of the embryos and juvenile fish. Moreover, the pretreatment of the oocyte with RU486 had a significant suppressive effect on the maternal mRNA transcript number of gr and igf system-related genes in oocytes and very early stage embryos, suggesting an action of antagonist on the stability of the maternal transcriptome.
Department of Biomedical Sciences, University of Guelph, Guelph, Ontario, Canada N1G 2W1.
Mao
M
Li
John F
JF
Leatherland
Matt M
MM
Vijayan
W Allan
WA
King
Pavneesh
P
Madan
D000818:Animals; D002455:Cell Division / Q000235:genetics / Q000502:physiology; D002970:Cleavage Stage, Ovum / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D004625:Embryo, Nonmammalian / Q000166:cytology* / Q000378:metabolism / Q000502:physiology; D005260:Female; D018507:Gene Expression Regulation, Developmental; D006854:Hydrocortisone / Q000032:analysis / Q000378:metabolism*; D017686:Oncorhynchus mykiss / Q000196:embryology / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D009865:Oocytes / Q000737:chemistry / Q000378:metabolism*; D011965:Receptors, Glucocorticoid / Q000819:agonists* / Q000378:metabolism / Q000502:physiology; D017451:Receptors, Somatomedin / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics; D013002:Somatomedins / Q000235:genetics* / Q000378:metabolism; D013997:Time Factors; D015854:Up-Regulation / Q000502:physiology; D015053:Zygote / Q000378:metabolism / Q000502:physiology*
D011965:Receptors, Glucocorticoid; D017451:Receptors, Somatomedin; D013002:Somatomedins; D006854:Hydrocortisone