-
BMC Genomics Feb 2019A key developmental transformation in the life of all vertebrates is the transition to sexual maturity, whereby individuals are capable of reproducing for the first...
BACKGROUND
A key developmental transformation in the life of all vertebrates is the transition to sexual maturity, whereby individuals are capable of reproducing for the first time. In the farming of Atlantic salmon, early maturation prior to harvest size has serious negative production impacts.
RESULTS
We report genome wide association studies (GWAS) using fish measured for sexual maturation in freshwater or the marine environment. Genotypic data from a custom 50 K single nucleotide polymorphism (SNP) array was used to identify 13 significantly associated SNP for freshwater maturation with the most strongly associated on chromosomes 10 and 11. A higher number of associations (48) were detected for marine maturation, and the two peak loci were found to be the same for both traits. The number and broad distribution of GWAS hits confirmed a highly polygenetic nature, and GWAS performed separately within males and females revealed sex specific genetic behaviour for loci co-located with positional candidate genes phosphatidylinositol-binding clathrin assembly protein-like (picalm) and membrane-associated guanylate kinase, WW and PDZ domain-containing protein 2 (magi2).
CONCLUSIONS
The results extend earlier work and have implications for future applied breeding strategies to delay maturation in this important aquaculture species.
Topics: Animals; Base Sequence; Breeding; Databases, Genetic; Female; Fisheries; Fresh Water; Gene Expression; Gene Frequency; Genetic Variation; Genome-Wide Association Study; Genotype; Guanylate Kinases; Male; Monomeric Clathrin Assembly Proteins; Multifactorial Inheritance; Polymorphism, Single Nucleotide; Salmo salar; Seawater; Sex Factors; Sexual Maturation; Tasmania; Whole Genome Sequencing
PubMed: 30770720
DOI: 10.1186/s12864-019-5525-4 -
Indian Pediatrics Jun 2006
Topics: Adolescent; Age Factors; Child; Female; Global Health; Humans; Male; Puberty; Puberty, Precocious; Rural Population; Sexual Maturation; Time Factors
PubMed: 16820656
DOI: No ID Found -
Poultry Science May 2021The 2 × 4 factorial experiment was designed to determine the effect of strain and photostimulation age on sexual maturity and reproductive performance of rooster...
The 2 × 4 factorial experiment was designed to determine the effect of strain and photostimulation age on sexual maturity and reproductive performance of rooster breeders. A total of 96 White Leghorn (WL) and 120 Beijing You Chicken (BYC) roosters were randomly allocated to 4 treatments at 14 wk of age. The treatments represent photostimulation at 16, 18, 20, and 22 wk of age, respectively (PS16, PS18, PS20, and PS22), in both strains. Photostimulation was achieved by increasing the day length from 8L:16D to 14L:10D and by increasing lighting intensity from 10 lx to 80 lx. Three birds from each interaction were sacrificed to characterize the comb and testis weights at 4 time points: 1 d before photostimulation and 2, 4, and 6 wk after photostimulation. Semen quality and hatching performance with the semen of the experimental roosters were measured at 30 and 45 wk of age, respectively. Results showed that the testis weight of PS20 and PS22 in WL and BYC was 6.4- and 2.9-fold higher than that of PS18 before photostimulation, while testis weight of PS18 in both strains increased sharply after photostimulation. The diameter of seminiferous tubules increased in the photostimulated roosters as compared with the nonphotostimulated ones, and mature spermatozoa were produced 4 wk after photostimulation and at 20 wk of age for PS16. The WL had lower semen volume and total sperm count than BYC (P < 0.01), but there was no difference on effective sperm count (P > 0.05). In addition, semen quality traits were not affected by age at photostimulation (P > 0.05) in both strains. The fertility and hatching performance were not affected by strain or photostimulation age (P > 0.05). In summary, the sexual maturation of rooster breeders can be advanced by photostimulation at an early age, which does not lead to a difference in semen quality or hatching performance at adult stage.
Topics: Animals; Chickens; Fertility; Male; Reproduction; Semen Analysis; Sexual Maturation
PubMed: 33752068
DOI: 10.1016/j.psj.2021.01.033 -
General and Comparative Endocrinology Sep 2022Age at maturity is a major contributor to the diversity of life history strategies in organisms. The process of maturation is influenced by both genetics and the...
Age at maturity is a major contributor to the diversity of life history strategies in organisms. The process of maturation is influenced by both genetics and the environment, and includes changes in levels of sex hormones and behavior, but the specific factors leading to variation in maturation timing are poorly understood. gnrh1 regulates the transcription of gonadotropin genes at pubertal onset in many species, but this gene is lacking in certain teleost species including Atlantic salmon (Salmo salar), which raises the possibility of the involvement of other important regulatory factors during this process. Earlier research has reported a strong association of alternative alleles of the vgll3 gene with maturation timing in Atlantic salmon, suggesting it as a potential candidate regulating reproductive axis genes. Here, we investigated the expression of reproductive axis genes in one-year-old Atlantic salmon males with immature gonads and different vgll3 genotypes during the spawning period. We detected strong vgll3 genotype-dependent differential expression of reproductive axis genes (such as fshb, lhb, amh and igf3) tested in the pituitary, and testis. In addition, we observed differential expression of jun (ap1) and nr5a1b (sf1), potential upstream regulators of gonadotropins in the pituitary, as well as axin2, id3, insl3, itch, ptgs2a and ptger4b, the downstream targets of amh and igf3 in the testis. Hereby, we provide evidence of strong vgll3 genotype-dependent transcriptional regulation of reproductive axis genes prior to sexual maturation and suggest alternative models for distinct actions of vgll3 genotypes on the related molecular processes.
Topics: Animals; Gene Expression; Genotype; Gonadotropins; Male; Salmo salar; Sexual Maturation; Transcription Factors
PubMed: 35580687
DOI: 10.1016/j.ygcen.2022.114055 -
Brain Research Jan 2017Postnatal brain development is studded with sensitive periods during which experience dependent plasticity is enhanced. This enables rapid learning from environmental... (Review)
Review
Postnatal brain development is studded with sensitive periods during which experience dependent plasticity is enhanced. This enables rapid learning from environmental inputs and reorganization of cortical circuits that matches behavior with environmental contingencies. Significant headway has been achieved in characterizing and understanding sensitive period biology in primary sensory cortices, but relatively little is known about sensitive period biology in associative neocortex. One possible mediator is the onset of puberty, which marks the transition to adolescence, when animals shift their behavior toward gaining independence and exploring their social world. Puberty onset correlates with reduced behavioral plasticity in some domains and enhanced plasticity in others, and therefore may drive the transition from juvenile to adolescent brain function. Pubertal onset is also occurring earlier in developed nations, particularly in unserved populations, and earlier puberty is associated with vulnerability for substance use, depression and anxiety. In the present article we review the evidence that supports a causal role for puberty in developmental changes in the function and neurobiology of the associative neocortex. We also propose a model for how pubertal hormones may regulate sensitive period plasticity in associative neocortex. We conclude that the evidence suggests puberty onset may play a causal role in some aspects of associative neocortical development, but that further research that manipulates puberty and measures gonadal hormones is required. We argue that further work of this kind is urgently needed to determine how earlier puberty may negatively impact human health and learning potential. This article is part of a Special Issue entitled SI: Adolescent plasticity.
Topics: Animals; Humans; Neocortex; Neuronal Plasticity; Puberty; Sexual Maturation
PubMed: 27590721
DOI: 10.1016/j.brainres.2016.08.042 -
Neuroendocrinology 2014All reproductively competent adults have gone through puberty. While key genes and signaling pathways that lead to the onset of sexual maturation are known, the... (Review)
Review
All reproductively competent adults have gone through puberty. While key genes and signaling pathways that lead to the onset of sexual maturation are known, the molecular mechanisms that determine when an individual enters puberty are only beginning to be understood. Both genetic and environmental factors determine the timing of puberty. New advances in understanding how environmentally sensitive, yet highly heritable developmental processes are regulated have come from the field of epigenetics. Of note, studies investigating the epigenetic control of the onset of puberty suggest that epigenetic repression of key inhibitory loci may play a fundamental role in the initiation of puberty. Current technologies that not only read out the DNA sequence, but also determine how the DNA is modified in response to the environment, promise new insight into how puberty is regulated, including the identification and understanding of gene regulatory networks that control the biological pathways affecting pubertal timing. Here we review the findings to date and discuss how epigenetic investigation can further our understanding of this fundamental aspect of human development.
Topics: Animals; Epigenesis, Genetic; Epigenomics; Humans; Puberty; Sexual Maturation
PubMed: 24718029
DOI: 10.1159/000362559 -
Hormones and Behavior Jul 2013This article is part of a Special Issue "Puberty and Adolescence". One of the defining characteristics of adolescence in humans is a large shift in the timing and... (Review)
Review
This article is part of a Special Issue "Puberty and Adolescence". One of the defining characteristics of adolescence in humans is a large shift in the timing and structure of sleep. Some of these changes are easily observable at the behavioral level, such as a shift in sleep patterns from a relatively morning to a relatively evening chronotype. However, there are equally large changes in the underlying architecture of sleep, including a >60% decrease in slow brain wave activity, which may reflect cortical pruning. In this review we examine the developmental forces driving adolescent sleep patterns using a cross-species comparison. We find that behavioral and physiological sleep parameters change during adolescence in non-human mammalian species, ranging from primates to rodents, in a manner that is often hormone-dependent. However, the overt appearance of these changes is species-specific, with polyphasic sleepers, such as rodents, showing a phase-advance in sleep timing and consolidation of daily sleep/wake rhythms. Using the classic two-process model of sleep regulation, we demonstrate via a series of simulations that many of the species-specific characteristics of adolescent sleep patterns can be explained by a universal decrease in the build-up and dissipation of sleep pressure. Moreover, and counterintuitively, we find that these changes do not necessitate a large decrease in overall sleep need, fitting the adolescent sleep literature. We compare these results to our previous review detailing evidence for adolescent changes in the regulation of sleep by the circadian timekeeping system (Hagenauer and Lee, 2012), and suggest that both processes may be responsible for adolescent sleep patterns.
Topics: Adolescent; Animals; Animals, Laboratory; Homeostasis; Humans; Psychology, Adolescent; Puberty; Sexual Maturation; Sleep
PubMed: 23998671
DOI: 10.1016/j.yhbeh.2013.01.013 -
Biology of Reproduction Jan 2019Acquisition of reproductive maturity involves one of the most important series of developmental events in an organism's life. The beginning of adolescence is marked by... (Review)
Review
Acquisition of reproductive maturity involves one of the most important series of developmental events in an organism's life. The beginning of adolescence is marked by the onset of puberty. Puberty is the continuum of physical changes through which an infantile body matures into an adult capable of reproduction. This is a period of increased brain plasticity, where processes of re-wiring, neuronal proliferation, and pruning are enhanced. The initiation of mammalian puberty requires an increased pulsatile release of gonadotropin-releasing hormone from the hypothalamus. Puberty is regulated by neuroendocrine, genetic, and epigenetic factors. The maturation and function of the reproductive axis are highly sensitive to the energy status of the organism and sophisticated mechanisms exist to inhibit the axis in unfavorable energetic or metabolic conditions.In this review, we will focus on the impact of alcohol and obesity on reproductive outcomes, with emphasis on their effects on the timing of puberty. In the case of obesity, conflictive data are found, and while in females the association of overnutrition with advanced onset of puberty is consistent, in males, discrepant results have been reported. Concerning alcohol exposure, compelling evidence has documented a delay in the onset of puberty. We will present here data from both clinical studies and research involving preclinical models, which do not only delineate the impact of these conditions on the timing of puberty and potential underlying mechanisms, but that may help to define better strategies for the rational management of puberty disorders, especially of metabolic origin.
Topics: Adolescent; Adult; Age of Onset; Alcohol Drinking; Animals; Ethanol; Female; Humans; Male; Pediatric Obesity; Puberty; Sexual Maturation; Time Factors
PubMed: 30052777
DOI: 10.1093/biolre/ioy168 -
Frontiers in Neuroendocrinology Apr 2019Gonadotropin releasing hormone (GnRH) is a highly conserved neuroendocrine decapeptide that is essential for the onset of puberty and the maintenance of the reproductive... (Review)
Review
Gonadotropin releasing hormone (GnRH) is a highly conserved neuroendocrine decapeptide that is essential for the onset of puberty and the maintenance of the reproductive state. First identified in mammals, the GnRH signaling pathway is found in all classes of vertebrates; homologues of GnRH have also been identified in invertebrates. In addition to its role as a hypothalamic releasing hormone, GnRH has multiple functions including modulating neural activity within specific regions of the brain. These various functions are mediated by multiple isoforms, which are expressed at diverse locations within the central nervous system. Here we discuss the GnRH signaling pathways in light of new reports that reveal that some vertebrate genomes lack GnRH1. Not only do other isoforms of GnRH not compensate for this gene loss, but elements upstream of GnRH1, including kisspeptins, appear to also be dispensable. We discuss routes that may compensate for the loss of the GnRH1 pathway.
Topics: Animals; Brain; Gonadotropin-Releasing Hormone; Humans; Kisspeptins; Neurons; Reproduction; Sexual Maturation
PubMed: 30797802
DOI: 10.1016/j.yfrne.2019.02.002 -
Journal of Animal Science Aug 2014Inappropriate programming of the reproductive system by developmental exposure to excess steroid hormones is of concern. Sheep are well suited for investigating... (Review)
Review
Inappropriate programming of the reproductive system by developmental exposure to excess steroid hormones is of concern. Sheep are well suited for investigating developmental origin of reproductive and metabolic disorders. The developmental time line of female sheep (approximately 5 mo gestation and approximately 7 mo to puberty) is ideal for conducting sequential studies of the progression of metabolic and/or reproductive disruption from the developmental insult to manifestation of adult consequences. Major benefits of using sheep include knowledge of established critical periods to target adult defects, a rich understanding of reproductive neuroendocrine regulation, availability of noninvasive approaches to monitor follicular dynamics, established surgical approaches to obtain hypophyseal portal blood for measurement of hypothalamic hormones, and the ability to perform studies in natural setting thereby keeping behavioral interactions intact. Of importance is the ability to chronically instrument fetus and mother for determining early endocrine perturbations. Prenatal exposure of the female to excess testosterone (T) leads to an array of adult reproductive disorders that include LH excess, functional hyperandrogenism, neuroendocrine defects, multifollicular ovarian morphology, and corpus luteum dysfunction culminating in early reproductive failure. At the neuroendocrine level, all 3 feedback systems are compromised. At the pituitary level, gonadotrope (LH secretion) sensitivity to GnRH is increased. Multifollicular ovarian morphology stems from persistence of follicles as well as enhanced follicular recruitment. These defects culminate in progressive loss of cyclicity and reduced fecundity. Prenatal T excess also leads to fetal growth retardation, an early marker of adult reproductive and metabolic diseases, insulin resistance, hypertension, and behavioral deficits. Collectively, the reproductive and metabolic deficits of prenatal T-treated sheep provide proof of concept for the developmental origin of fertility and metabolic disorders. Studies with the environmental endocrine disruptor bisphenol A (BPA) show that reproductive disruptions found in prenatal BPA-treated sheep are similar to those seen in prenatal T-treated sheep. The ubiquitous exposure to endocrine disrupting compounds with steroidogenic potential via the environment and food sources calls for studies addressing the impact of developmental exposure to environmental steroid mimics on reproductive function.
Topics: Animals; Benzhydryl Compounds; Endocrine Disruptors; Female; Fertility; Metabolic Diseases; Ovary; Phenols; Pregnancy; Prenatal Exposure Delayed Effects; Reproduction; Sexual Maturation; Sheep; Testosterone
PubMed: 25074449
DOI: 10.2527/jas.2014-7637