Abstract

BackgroundHigh egg producing hens (HEPH) show increased hypothalamic and pituitary gene expression related to hypothalamo-pituitary-gonadal (HPG) axis stimulation as well as increased in vitro responsiveness to gonadotropin releasing hormone (GnRH) stimulation in the pituitary when compared to low egg producing hens (LEPH). Transcriptome analysis was performed on hypothalamus and pituitary samples from LEPH and HEPH to identify novel regulators of HPG axis function.ResultsIn the hypothalamus and pituitary, 4644 differentially expressed genes (DEGs) were identified between LEPH and HEPH, with 2021 genes up-regulated in LEPH and 2623 genes up-regulated in HEPH. In LEPH, up-regulated genes showed enrichment of the hypothalamo-pituitary-thyroid (HPT) axis. Beta-estradiol was identified as an upstream regulator regardless of tissue. When LEPH and HEPH samples were compared, beta-estradiol was activated in HEPH in 3 of the 4 comparisons, which correlated to the number of beta-estradiol target genes up-regulated in HEPH. In in vitro pituitary cell cultures from LEPH and HEPH, thyroid hormone pretreatment negatively impacted gonadotropin subunit mRNA levels in cells from both LEPH and HEPH, with the effect being more prominent in HEPH cells. Additionally, the effect of estradiol pretreatment on gonadotropin subunit mRNA levels in HEPH cells was negative, whereas estradiol pretreatment increased gonadotropin subunit mRNA levels in LEPH cells.ConclusionsUp-regulation of the HPT axis in LEPH and upstream beta-estradiol activation in HEPH may play a role in regulating HPG axis function, and ultimately ovulation rates. Thyroid hormone and estradiol pretreatment impacted gonadotropin mRNA levels following GnRH stimulation, with the inhibitory effects of thyroid hormone more detrimental in HEPH and estradiol stimulatory effects more prominent in LEPH. Responsiveness to thyroid hormone and estradiol may be due to desensitization to thyroid hormone and estradiol in LEPH and HEPH, respectively, due to up-regulation of the HPT axis in LEPH and of the HPG axis in HEPH. Further studies will be necessary to identify possible target gene desensitization mechanisms and elicit the regulatory role of the HPT axis and beta-estradiol on ovulation rates in turkey hens.

Highlights

  • High egg producing hens (HEPH) show increased hypothalamic and pituitary gene expression related to hypothalamo-pituitary-gonadal (HPG) axis stimulation as well as increased in vitro responsiveness to gonadotropin releasing hormone (GnRH) stimulation in the pituitary when compared to low egg producing hens (LEPH)

  • In the hypothalamus and pituitary, under both ovulatory cycle conditions, unannotated genes accounted for roughly 20–30% of the differentially expressed genes (DEGs), indicating that further progress annotating the turkey genome may reveal additional genes involved in egg production rates or in triggering ovulation

  • Thyroid hormone pretreatment (T3) negatively regulated gonadotropin production, independent of GnRH treatment concentration, with a higher negative response from high egg producing hens (HEPH). These findings suggest that HEPH are more sensitive to the effect of T3 on gonadotropin production, whereas LEPH are more resistant to the effects of T3

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Summary

Introduction

High egg producing hens (HEPH) show increased hypothalamic and pituitary gene expression related to hypothalamo-pituitary-gonadal (HPG) axis stimulation as well as increased in vitro responsiveness to gonadotropin releasing hormone (GnRH) stimulation in the pituitary when compared to low egg producing hens (LEPH). Egg production is regulated by the hypothalamo-pituitary-gonadal (HPG) axis. Proper function of the HPG axis involves feedback on the hypothalamus and pituitary by gonadal steroid hormones and can be impacted by inputs from other neuroendocrine axes, such as the hypothalamo-pituitarythyroid (HPT) axis. Progesterone feedback on the hypothalamus and pituitary triggers a preovulatory surge (PS) of luteinizing hormone (LH) and progesterone, resulting in follicle ovulation, but the role of estradiol feedback during the PS is not well characterized in the turkey hen. Estradiol reduces gonadotropin inhibitory hormone (GnIH) production and exerts positive and negative feedback on gonadotropin releasing hormone (GnRH) production in the hypothalamus, indicating that estradiol feedback may play a role in ovulation timing [1, 2]

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