The current study is designed to characterize the ontogeny of dactylin expression in the developing mouse embryo. Dactylin is an important gene for proper digit formation. It is a member of the F‐box/WD40 gene family and is involved in the ubiquitin ligase process that targets specific proteins for degradation. Mouse dactylaplasia has similar phenotypic characteristics to humans with split hand/ spilt foot malformation, furthermore dactylin, which has been mapped to chromosome 19 in mice, is syntenic to the SHFM3 region in humans on chromsome 10q24. Understanding the ontogeny of dactylin is important because it allows us to look at specific time periods critical for the development of digits. Mouse embryos were collected prior to digit formation (E8 and E10), during digit formation (E12), and after digit formation is complete (E14) to determine at what point dactylin expression was turned on and off. Once the embryos were collected the limb buds or entire limbs were removed, total mRNA isolated, and RT‐PCR was used to determine gene expression. We found dactylin expression to be present at all time periods examined. In order to get a more complete ontogeny, we are currently expanding the original time frame to E2 through E21. This work was supported by a Lander University Foundation Grant.
The effects of kisspeptin on reproductive development have been well‐documented in the past decade. More recently, a mammalian orthologue of Gonadotrophin Inhibitory Hormone (GnIH), known as RF‐amide‐related‐peptide‐3 (RFRP3), has also been found to affect reproductive function. It has been proposed that GnIH antagonizes the effect of KISS‐1that upregulates the reproductive system during puberty. In the current study, differential expression of kisspeptin and RFRP3 were examined in the hypothalamic of female rats at various stages of postnatal development. Hypothalamic samples from rats at days 10, 20, 30, 40, 50, and 60 were examined for gene expression of GnRH, GnIH, KISS‐1 and the receptors GPR147 and GPR54. GnRH was expressed very early and its expression was maintained throughout the experiment. GnIH and KISS‐1 expression was greatest on day 30 and then declined during the transition into puberty. These data suggest that perhaps GnIH is up‐regulated once the hypothalamus has fully developed and is prepared for reproduction but is inhibiting reproductive function until other signals from the reproductive axis provide feedback that oogenesis is also complete. This research was supported by the Lander University Foundation Grant.
While leptin and kisspeptin have both been implicated in the onset of puberty in mammals, the pathway linking leptin and kisspeptin is still not completely understood. Such knowledge could play an important role in treating or preventing infertility, both in humans, for the purpose of child bearing, and in other mammals, for agricultural reasons. Recent studies have suggested that mTOR, a ubiquitous serine/threonine kinase involved in cell and tissue growth and also a target of leptin signaling in the paraventricular and arcuate nuclei of the hypothalamus, may act as a signaling intermediate in the leptin‐kisspeptin pathway. Therefore, increases in mTOR in the hypothalamus may correlate with increases of leptin and kisspeptin in the hypothalamus as well. In this experiment, the gene expression of leptin, kisspeptin, and mTOR were examined using reverse‐transcriptase and polymerase chain reaction (RT‐PCR) from the hypothalami of female rats in ten day intervals beginning on postnatal day‐10 through postnatal day‐60. An increase in mTOR expression at day 40 correlated with increased expression in both leptin and kisspeptin. These findings suggest that mTOR could be involved in the leptin‐kisspeptin pathway and, therefore, the onset of puberty. This research was supported by a Lander University Foundation Grant.
Follicle‐stimulating hormone (FSH) is a glycoprotein secreted from the anterior pituitary. Like other glycoproteins, FSH exists as a mixture of isoforms that vary in the number and type of sugar groups. Observed changes in FSH isoforms during critical reproductive events, such as puberty onset, suggest that different combinations of FSH isoforms influence reproduction differently. It has also been suggested that all FSH isoforms may not equally bind to antibody based assays. In order to establish a working model, a study was performed using pre‐pubertal mice to determine at what age FSH mRNA expression begins. Gene expression was determined for the alpha, FSH beta, LH beta, and TSH beta subunits in five‐, ten‐, fifteen‐, twenty‐, thirty‐, and sixty‐day‐old mice. All subunits were expressed in all age groups indicating that FSH expression begins very early in development. However, despite the expression of mRNA, morphological studies do not reflect an active form of FSH is initiating gonad development, hormone production, or gametogenesis. Early expression of FSH may be critical to establish a hormonal milieu that leads to maturation of the gonads. Another possibility is that different isoforms of FSH determine its physiological significance during different metabolic states.
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