scholarly journals Transcriptional sexual dimorphism during preimplantation embryo development and its consequences for developmental competence and adult health and disease

Reproduction ◽  
2011 ◽  
Vol 141 (5) ◽  
pp. 563-570 ◽  
Author(s):  
P Bermejo-Alvarez ◽  
D Rizos ◽  
P Lonergan ◽  
A Gutierrez-Adan
Keyword(s):  
Sexual Dimorphism ◽  
Sex Chromosome ◽  
Developmental Competence ◽  
Preimplantation Embryos ◽  
Adult Health ◽  
Long Term Effects ◽  
Preimplantation Embryo Development ◽  
Phenotypic Differences ◽  
Hormone Effects ◽  
Health And Disease

In adult tissues, sexual dimorphism is largely attributed to sex hormone effects, although there is increasing evidence for a major role of sex chromosome dosage. During preimplantation development, male and female embryos can display phenotypic differences that can only be attributed to the transcriptional differences resulting from their different sex chromosome complements. Thus, all expressed Y-linked genes and those X-linked genes that totally or partially escape X-chromosome inactivation at each specific developmental stage display transcriptional sexual dimorphism. Furthermore, these differentially expressed sex chromosome transcripts can regulate the transcription of autosomal genes, leading to a large transcriptional sexual dimorphism. The sex-dependent transcriptional differences may affect several molecular pathways such as glucose metabolism, DNA methylation and epigenetic regulation, and protein metabolism. These molecular differences may have developmental consequences, including sex-selective embryo loss and sex-specific epigenetic responses to environmental hazards, leading to long-term effects. This review discusses transcriptional sexual dimorphism in preimplantation embryos, its consequences on sex ratio biases and on the developmental origin of health and disease, and its significance for transcriptional studies and adult sexual dimorphism.

Sex-specific embryonic origin of postnatal phenotypic variability

2013 ◽  
Vol 25 (1) ◽  
pp. 38 ◽  
Author(s):  
R. Laguna-Barraza ◽  
P. Bermejo-Álvarez ◽  
P. Ramos-Ibeas ◽  
C. de Frutos ◽  
A. P. López-Cardona ◽  
...  
Keyword(s):  
Sex Ratio ◽  
Environmental Conditions ◽  
Developmental Plasticity ◽  
Current Knowledge ◽  
Phenotypic Variability ◽  
Early Embryo ◽  
Preimplantation Embryos ◽  
Adult Health ◽  
Long Term Effects

Preimplantation developmental plasticity has evolved in order to offer the best chances of survival under changing environments. Conversely, environmental conditions experienced in early life can dramatically influence neonatal and adult biology, which may result in detrimental long-term effects. Several studies have shown that small size at birth, which is associated with a greater risk of metabolic syndrome, is largely determined before the formation of the blastocysts because 70%–80% of variation in bodyweight at birth has neither a genetic nor environmental component. In addition, it has been reported that adult bodyweight is programmed by energy-dependent process during the pronuclear stage in the mouse. Although the early embryo has a high developmental plasticity and adapts and survives to adverse environmental conditions, this adaptation may have adverse consequences and there is strong evidence that in vitro culture can be a risk factor for abnormal fetal outcomes in animals systems, with growing data suggesting that a similar link may be apparent for humans. In this context, male and female preimplantation embryos display sex-specific transcriptional and epigenetic regulation, which, in the case of bovine blastocysts, expands to one-third of the transcripts detected through microarray analysis. This sex-specific bias may convert the otherwise buffered stochastic variability in developmental networks in a sex-determined response to the environmental hazard. It has been widely reported that environment can affect preimplantation development in a sex-specific manner, resulting in either a short-term sex ratio adjustment or in long-term sex-specific effects on adult health. The present article reviews current knowledge about the natural phenotypic variation caused by epigenetic mechanisms and the mechanisms modulating sex-specific changes in phenotype during early embryo development resulting in sex ratio adjustments or detrimental sex-specific consequences for adult health. Understanding the natural embryo sexual dimorphism for programming trajectories will help understand the early mechanisms of response to environmental insults.

scholarly journals Long-Term Effects of Abuse in Later Life Perpetrated by Family Members

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 444-445
Author(s):  
Naomi Meinertz ◽  
Pi-Ju Liu ◽  
Ron Acierno
Keyword(s):  
Social Support ◽  
Depressive Symptoms ◽  
Family Member ◽  
Older Adult ◽  
Family Members ◽  
Later Life ◽  
Adult Health ◽  
Long Term Effects ◽  
Long Term Impact

Abstract Abuse in later life could potentially lead to lower levels of social support, especially when perpetrated by family members who are charged with protecting the older adult in their care. Using both waves of the National Elder Mistreatment longitudinal data (wave one collected in 2008 and wave two in 2015; N=774), long-term effects of abuse (i.e., physical, emotional, sexual, and financial) on levels of social support, physical health, and clinical depressive symptoms for respondents at or above the age of 60 years were analyzed. A multivariate analysis of variance showed that respondents abused at wave one (n=261) by a family member (B=-0.55, p≤0.001), a spouse or ex-partner (B=-0.349, p=0.02), or a non-relative or stranger (B=-0.301, p=0.026) had lower levels of social support eight years later at wave two. Those abused by a family member at wave one also experienced higher levels of depressive symptoms at wave two (B=-0.187, p=0.01). Perpetrator type did not predict general health at wave two. These results emphasize the long-term impact of abuse on the lives of older adults and highlight the importance trusted relationships, such as with family members, have on older adult health and wellbeing.

scholarly journals Inhibition of DRP1 Impedes Zygotic Genome Activation and Preimplantation Development in Mice

2021 ◽  
Vol 9 ◽  
Author(s):  
Yuanyuan Li ◽  
Ning-Hua Mei ◽  
Gui-Ping Cheng ◽  
Jing Yang ◽  
Li-Quan Zhou
Keyword(s):  
Embryo Development ◽  
Preimplantation Embryo ◽  
Preimplantation Embryos ◽  
Dependent Manner ◽  
Zygotic Genome Activation ◽  
Preimplantation Embryo Development ◽  
Cell Embryo ◽  
Embryo Stage ◽  
Genome Activation ◽  
Zygotic Genome

Mitochondrion plays an indispensable role during preimplantation embryo development. Dynamic-related protein 1 (DRP1) is critical for mitochondrial fission and controls oocyte maturation. However, its role in preimplantation embryo development is still lacking. In this study, we demonstrate that inhibition of DRP1 activity by mitochondrial division inhibitor-1, a small molecule reported to specifically inhibit DRP1 activity, can cause severe developmental arrest of preimplantation embryos in a dose-dependent manner in mice. Meanwhile, DRP1 inhibition resulted in mitochondrial dysfunction including decreased mitochondrial activity, loss of mitochondrial membrane potential, reduced mitochondrial copy number and inadequate ATP by disrupting both expression and activity of DRP1 and mitochondrial complex assembly, leading to excessive ROS production, severe DNA damage and cell cycle arrest at 2-cell embryo stage. Furthermore, reduced transcriptional and translational activity and altered histone modifications in DRP1-inhibited embryos contributed to impeded zygotic genome activation, which prevented early embryos from efficient development beyond 2-cell embryo stage. These results show that DRP1 inhibition has potential cytotoxic effects on mammalian reproduction, and DRP1 inhibitor should be used with caution when it is applied to treat diseases. Additionally, this study improves our understanding of the crosstalk between mitochondrial metabolism and zygotic genome activation.

scholarly journals Homage to the ‘H’ in developmental origins of health and disease

2016 ◽  
Vol 8 (1) ◽  
pp. 8-29 ◽  
Author(s):  
C. S. Rosenfeld
Keyword(s):  
Female Offspring ◽  
Postnatal Period ◽  
Environmental Chemicals ◽  
Primary Concern ◽  
Developmental Origins ◽  
Adult Health ◽  
Fetal Origins ◽  
Adult Disease ◽  
Remediation Strategies ◽  
Health And Disease

Abundant evidence exists linking maternal and paternal environments from pericopconception through the postnatal period to later risk to offspring diseases. This concept was first articulated by the late Sir David Barker and as such coined the Barker Hypothesis. The term was then mutated to Fetal Origins of Adult Disease and finally broadened to developmental origins of adult health and disease (DOHaD) in recognition that the perinatal environment can shape both health and disease in resulting offspring. Developmental exposure to various factors, including stress, obesity, caloric-rich diets and environmental chemicals can lead to detrimental offspring health outcomes. However, less attention has been paid to date on measures that parents can take to promote the long-term health of their offspring. In essence, have we neglected to consider the ‘H’ in DOHaD? It is the ‘H’ component that should be of primary concern to expecting mothers and fathers and those seeking to have children. While it may not be possible to eliminate exposure to all pernicious factors, prevention/remediation strategies may tip the scale to health rather than disease. By understanding disruptive DOHaD mechanisms, it may also illuminate behavioral modifications that parents can adapt before fertilization and throughout the neonatal period to promote the lifelong health of their male and female offspring. Three possibilities will be explored in the current review: parental exercise, probiotic supplementation and breastfeeding in the case of mothers. The ‘H’ paradigm should be the focus going forward as a healthy start can indeed last a lifetime.

Self-reported physical health status of donor sperm-conceived adults

2020 ◽  
pp. 1-14
Author(s):  
Damian H. Adams ◽  
Adam Gerace ◽  
Michael J. Davies ◽  
Sheryl de Lacey
Keyword(s):  
Health Outcomes ◽  
Acute Bronchitis ◽  
Sleep Apnoea ◽  
Developmental Origins ◽  
Adult Health ◽  
Physical Health Status ◽  
Donor Sperm ◽  
Health And Disease

Abstract Donor-conceived neonates have poorer birth outcomes, including low birth weight and preterm delivery that are associated with poorer long-term health in adulthood through the developmental origins of health and disease (DOHaD) theory. The aim of this study was to conduct the first investigation of the adult health outcomes of donor-conceived people. An online health survey was completed by 272 donor sperm-conceived adults and 877 spontaneously conceived adults from around the world. Donor and spontaneously conceived groups were matched for age, sex, height, smoking, alcohol consumption, exercise, own fertility and maternal smoking. Donor sperm-conceived adults had significantly higher reports of being diagnosed with type 1 diabetes (P = 0.031), thyroid disease (P = 0.031), acute bronchitis (P = 0.008), environmental allergies (P = 0.046), sleep apnoea (P = 0.037) and having ear tubes/grommets surgically implanted (P = 0.046). This is the first study to investigate the health outcomes of adult donor sperm-conceived people. Donor sperm-conceived adults self-reported elevated frequencies of various health conditions. The outcomes are consistent with birth defect data from donor sperm treatment and are consistent with the DOHaD linking perturbed early growth and chronic disease in adulthood.

scholarly journals Developmental competence and oxidative state of mouse zygotes heat-stressed maternally or in vitro

Reproduction ◽  
2002 ◽  
pp. 683-689 ◽  
Author(s):  
M Ozawa ◽  
M Hirabayashi ◽  
Y Kanai
Keyword(s):  
Hydrogen Peroxide ◽  
Heat Stress ◽  
Mouse Embryos ◽  
Developmental Competence ◽  
Preimplantation Embryos ◽  
Physiological Changes ◽  
Cleavage Rate ◽  
Maternal Environment ◽  
Stressed Group

Mammalian preimplantation embryos are sensitive to maternal and direct heat stress. However, the mechanisms by which heat stress affects early embryonic development in vivo or in vitro are unknown. This study examined whether heat-stress-induced loss of developmental competence in mouse embryos was mediated by physiological changes in the maternal environment or by high temperatures alone. After fertilization, zygotes at the same stage were heat-stressed at 39.5 degrees C for 12 h either maternally (measured by maternal rectal temperature) or directly in culture. Zygotes in each group were cultured at 37.5 degrees C for a further 84 h to assess their developmental ability. Neither type of heat stress affected the first cleavage rate. However, the proportion of embryos that developed to morulae or blastocysts was significantly lower in the maternally heat-stressed group, but not in the directly heat-stressed group. Moreover, maternal heat stress significantly reduced intracellular glutathione concentrations and enhanced hydrogen peroxide concentrations in both zygotes and two-cell embryos that were recovered immediately after heat stress or 12 h later, respectively. In contrast, direct heat stress had little effect on concentrations of glutathione or hydrogen peroxide in cultured early embryos. These results demonstrate that maternal heat stress at the zygote stage reduces the developmental ability of mouse embryos via physiological changes in the maternal environment that lead to an increase in intracellular oxidative stress on the embryo.

Sex chromosome complement involvement in angiotensin receptor sexual dimorphism

2017 ◽  
Vol 447 ◽  
pp. 98-105 ◽  
Author(s):  
Florencia M. Dadam ◽  
Carla D. Cisternas ◽  
Ana F. Macchione ◽  
Andrea Godino ◽  
José Antunes-Rodrigues ◽  
...  
Keyword(s):  
Sexual Dimorphism ◽  
Sex Chromosome ◽  
Chromosome Complement ◽  
Angiotensin Receptor

scholarly journals Amino acid depletion and appearance during porcine preimplantation embryo development in vitro

Reproduction ◽  
2005 ◽  
Vol 130 (5) ◽  
pp. 655-668 ◽  
Author(s):  
Paul J Booth ◽  
Peter G Humpherson ◽  
Terry J Watson ◽  
Henry J Leese
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Embryo Development ◽  
Preimplantation Embryos ◽  
Type I ◽  
Preimplantation Embryo Development ◽  
Type Iv ◽  
Stage Of Development ◽  
Amino Acid Depletion

Preimplantation embryos can consume and produce amino acids in a manner dependent upon the stage of development that may be predictive of subsequent viability. In order to examine these relationships in the pig, patterns of net depletion and appearance of amino acids byin vitroproduced porcine preimplantation embryos were examined. Cumulus oocyte complexes derived from slaughterhouse pre-pubertal pig ovaries were matured for 40 h in defined TCM-199 medium (containing PVA) before being fertilised (Day 0) with frozen-thawed semen in Tris–based medium. After 6 h, presumptive zygotes were denuded and cultured in groups of 20, in NCSU-23 medium modified to contain 0.1 mM glutamine plus a mixture of 19 amino acids (aa) at low concentrations (0.02–0.11 mM) (NCSU-23aa). Groups of 2–20 embryos were removed (dependent on stage) on Day 0 (1 cell), Day 1 (two- and four-cells), Day 4 (compact morulae) and Day 6 (blastocysts) and placed in 4 μl NCSU-23aafor 24 h. After incubation, the embryos were removed and the spent media was analysed by HPLC. The net rate of amino acid depletion or appearance varied according to amino acid (P< 0.001) and, apart from serine and histidine, stage of development (P< 0.014). Glycine, isoleucine, valine, phenylalanine, tryptophan, methionine, asparagine, lysine, glutamate and aspartate consistently appeared, whereas threonine, glutamine and arginine were consistently depleted. Five types of stage-dependent trends could be observed: Type I: amino acids having high rates of net appearance on Day 0 that reached a nadir on Day 1 or 4 but subsequently increased by Day 6 (glycine, glutamate); Type II: those that exhibited lower rates of net appearance on Days 0 and 6 compared with the intermediate Days 1 and 4 (isoleucine, valine, phenylalanine, methionine, arginine); Type III: amino acids which showed a continuous fall in net appearance (asparagine, aspartate); Type IV: those that exhibited a steady fall in net depletion from Day 0 to Day 6 (glutamine, threonine); Type V: those following no discernable trend. Analysis of further embryo types indicated that presumptive polyspermic embryos on Day 0 had increased (P< 0.05) net rates of leucine, isoleucine, valine and glutamate appearance, and reduced (P< 0.05) net rates of threonine and glutamine depletion compared with normally inseminated oocytes. These data suggest that the net rates of depletion and uptake of amino acids by pig embryos vary between a) amino acids, b) the day of embryo development and, c) the type of embryos present at a given stage of development. The results also suggested that the net depletion and appearance rates of amino acids by early pig embryos might be more similar to those of the human than those of the mouse and cow.

035. Circadian rhythms and the early life programming of adult physiological systems

2005 ◽  
Vol 17 (9) ◽  
pp. 71
Author(s):  
D. J. Kennaway
Keyword(s):  
Circadian Rhythms ◽  
Neural Development ◽  
Optimal Time ◽  
Adult Health ◽  
Metabolic Dysfunction ◽  
Long Term Effects ◽  
Peripheral Tissues ◽  
Clock System ◽  
The Impact ◽  
Physiological Systems

We are all familiar with the idea that the external environment influences many diverse physiological systems. For example, the level of nutrition can not only influence adult health directly, but also fetal development and subsequently many adult functions in the offspring. Maternal stress can affect fetal outcomes as can the administration of drugs during pregnancy. Until recently, however, the daily changes in environmental light have been considered to really only influence the time that we sleep and in many other species the optimal time to mate. The impact of circadian rhythms on life trajectory has had little attention. In the last 5 years it has become clear that circadian rhythmicity is entrenched in virtually every cell of our bodies. A suite of clock gene transcription factors that include Clock, Bmal1 and the period and cryptochrome genes, generate a robust daily cycle of transcription and translation of hundreds of proteins. This cellular clock system is synchronised with the external photoperiod through retinal light perception, the hypothalamic suprachiasmatic nucleus (SCN) and neural and hormonal pathways. Most importantly when the clock system in peripheral tissues is disrupted, a growing list of detrimental consequences are being uncovered. As an example, mice with mutations in either Clock or Bmal1 have non-rhythmic peripheral tissues and exhibit mild to severe reproductive failure and metabolic dysfunction. Null per2 mice have a higher incidence of salivary gland hyperplasia, teratomas and increased susceptibility to radiation induced lymphomas. It is also apparent that intrauterine insults (e.g. cocaine administration, poor nutrition and stress) can have long term effects on the central circadian timing system in the SCN. Whether this involves alterations in neural development or gene function is not known. Nevertheless it is time we paid more attention to the temporal nature of our environment as a possible contributor to lifetime disorders and diseases.

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