In this review, we describe the process of sexual maturation in the bull calf. The testes of the bull grow relatively slowly until approximately 25 weeks of age and then a rapid phase of growth occurs until puberty, at 37-50 weeks of age. During the early postnatal phase of slower growth of the testis pre-spermatogonia and some spermatogonia are established, adult Leydig cells appear and undifferentiated Sertoli cells are produced. The rapid testicular growth, after 25 weeks of age, consists of marked increases in the diameter and length of the seminiferous tubules, dramatic proliferation and differentiation of germ cells, with mature spermatozoa occurring between 32 and 40 weeks of age. The adult Leydig cell population is largely in place by 30 weeks of age and that of Sertoli cells by 30-40 weeks of age. Serum concentrations of LH increase from 4 to 5 weeks of age, to an early postnatal peak at 12-16 weeks of age, followed by a decline to 25 weeks of age. Serum FSH concentrations are high postnatally, declining to approximately 25 weeks of age. Serum testosterone concentrations increase during the phase of rapid testicular growth. Hypothalamic opioidergic inhibition may abate transiently to allow the early postnatal increase in LH secretion, while testicular androgenic negative feedback probably contributes to the decline in gonadotropin secretion to 25 weeks of age. Several lines of study have led us to suggest that early postnatal gonadotropin secretion is pivotal in initiating the process of sexual maturation in the bull calf.
In the ewe, ovarian follicular waves emerge every 4 to 5 days and are preceded by a peak in FSH secretion. It is unclear whether large antral follicle(s) in a wave suppress the growth of other smaller follicles during the inter-wave interval, as is seen in cattle. In this study, anestrous (n = 6; experiment 1) and cyclic (n = 5; experiment 2) Western white face ewes were given ovine FSH (oFSH) (0.5 microg/kg; two s.c. injections, 8 h apart) during the growth phase (based on ultrasonography) of a follicular wave (wave 1). Control ewes (n = 5 and 6, respectively) received vehicle. In oFSH-treated ewes, serum FSH concentrations reached a peak (P < 0.05) by 12 h after oFSH treatment, and this induced FSH peak did not differ (P > 0.05) from the endogenous FSH peaks. In all ewes, emergence of follicular waves 1 and 2 was seen (P > 0.05). However, in oFSH-treated ewes, an additional follicular wave emerged approximately 0.5 days after treatment: during the interwave interval of waves 1 and 2 without delaying the emergence of wave 2. The growth characteristics and serum estradiol concentrations did not differ (P > 0.05) between oFSH-induced waves and waves induced by endogenous FSH peaks. We concluded that, unlike in cattle, the largest follicle of a wave in sheep has limited direct effect on the growth of other follicles induced by exogenous oFSH. In addition, the largest follicle of a wave may possibly not influence the rhythmicity of follicular wave emergence, as it does in cattle.
The primary objectives of this study were to follow the temporal patterns of testicular LH and FSH receptor (LH-R and FSH-R) concentrations and affinity (K a ) during sexual maturation in bulls and to see if such patterns could help explain the control of rapid testicular growth that occurs after 25 weeks of age, when serum gonadotropin concentrations are low. Separate groups of Hereford!Charolais calves (nZ6) were castrated every 4 weeks from 5 to 33 weeks of age and at 56 weeks of age. A week prior to castrations, from 5 to 33 weeks of age, blood was collected every 15 min for 10 h. The transition from indifferent supporting cells to Sertoli cells in seminiferous tubules was rapid between 13 and 25 weeks and rapid testis growth occurred after 25 weeks of age. Serum LH and FSH concentrations were transiently elevated at 12 weeks of age (P!0.05). LH-R concentrations decreased from 13 to 25 weeks of age and increased to 56 weeks of age (P!0.05). LH-RK a decreased from 9 to 17 weeks of age, increased to 29 weeks of age and declined to 33 weeks of age (P!0.05). FSH-R concentrations declined from 17 to 25 weeks of age then increased to 56 weeks of age (P!0.05). FSH-RK a increased from 17 to 25 weeks of age (P!0.05). High concentrations of gonadotropins and their receptors may be critical to initiate testis growth postnatally and support it after 25 weeks of age in the face of low serum gonadotropin concentrations.
Adolescent Idiopathic Scoliosis (AIS) is a spinal deformity that affects approximately 3 percent of human adolescents. Although the etiology and molecular basis of AIS is unclear, several genes such as POC5 have been identified as possible causes of the condition. In order to understand the role of POC5 in the pathogenesis of AIS, we investigated the subcellular localization of POC5 in cilia of cells over-expressing either the wild type (wt) or an AIS-related POC5 variant POC5 A429V . Mutation of POC5 was found to alter its subcellular localization and to induce ciliary retraction. Furthermore, we observed an impaired cell-cycle progression with the accumulation of cells in the S-phase in cells expressing POC5 A429V . Using immunoprecipitation coupled to mass spectrometry, we identified specific protein interaction partners of POC5, most of which were components of cilia and cytoskeleton. Several of these interactions were altered upon mutation of POC5. Altogether, our results demonstrate major cellular alterations, disturbances in centrosome protein interactions and cilia retraction in cells expressing an AIS-related POC5 mutation. Our study suggests that defects in centrosomes and cilia may underlie AIS pathogenesis.
The human fyn-related kinase (FRK) is a non-receptor tyrosine kinase known to have tumor suppressor activity in breast cancer cells. However, its mechanism of action has not been fully characterized. We generated FRK-stable MDA-MB-231 breast cancer cell lines and analyzed the effect on cell proliferation, migration, and invasiveness. We also used kinome analysis to identify potential FRK-regulated signaling pathways. We employed both immunoblotting and RT-PCR to identify/validate FRK-regulated targets (proteins and genes) in these cells. Finally, we interrogated the TCGA and GENT gene expression databases to determine the correlation between the expression of FRK and epithelial/mesenchymal markers. We observed that FRK overexpression suppressed cell proliferation, migration, and invasiveness, inhibited various JAK/STAT, MAPK and Akt signaling pathways, and suppressed the expression of some STAT3 target genes. Also, FRK overexpression increased the expression of epithelial markers including E-cadherin mRNA and down-regulated the transcript levels of vimentin, fibronectin, and slug. Finally, we observed an inverse correlation between FRK expression and mesenchymal markers in a large cohort of breast cancer cells. Our data, therefore, suggests that FRK represses cell proliferation, migration and invasiveness by suppressing epithelial to mesenchymal transition.
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