Mechanisms of sexually dimorphic adipose tissue remodelling upon prolonged breastfeeding
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE306420 | GEO | 2025/09/01
REPOSITORIES: GEO
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Project description:Mechanisms of sexually dimorphic adipose tissue remodelling upon prolonged breastfeeding
| PRJNA1310593 | ENA
Project description:All organisms with sexual reproduction undergo a process of mating, which essentially involves the encounter of two individuals belonging to different sexes. During mate search, both sexes should mutually optimize their encounters, thus raising a question of how they achieve this. Here, we show that a population with sexually dimorphic movement patterns achieves the highest individual mating success under a limited lifespan. Extensive simulations found and analytical approximations corroborated the existence of conditions under which sexual dimorphism in the movement patterns (i.e. how diffusively they move) is advantageous over sexual monomorphism. Mutual searchers with limited lifespans need to balance the speed and accuracy of finding their mates, and dimorphic movements can solve this trade-off. We further demonstrate that the sexual dimorphism can evolve from an initial sexually monomorphic population. Our results emphasize the importance of considering mutual optimization in problems of random search.
| S-EPMC5454297 | biostudies-literature
Project description:Sex hormones such as estrogen and testosterone are essential for sexually dimorphic behaviors in vertebrates. However, the hormone-activated molecular mechanisms that control the development and function of the underlying neural circuits remain poorly defined. We have identified numerous sexually dimorphic gene expression patterns in the adult mouse hypothalamus and amygdala. We find that adult sex hormones regulate these expression patterns in a sex-specific, regionally restricted manner, suggesting that these genes regulate sex typical behaviors. Indeed, we find that mice with targeted disruptions of each of four of these genes (Brs3, Cckar, Irs4, Sytl4) exhibit extremely specific deficits in sex specific behaviors, with single genes controlling the pattern or extent of male sexual behavior, male aggression, maternal behavior, or female sexual behavior. Taken together, our findings demonstrate that various components of sexually dimorphic behaviors are governed by separable genetic programs.
| S-EPMC3326403 | biostudies-literature
Project description:The scientific understanding of fear and anxiety-in both normal and pathological forms-is presently limited by a predominance of studies that use male animals and Pavlovian fear conditioning-centered paradigms that restrict and assess specific behaviors (e.g., freezing) over brief sampling periods and overlook the broader contributions of the spatiotemporal context to an animal's behavioral responses to threats. Here, we use a risky "closed economy" system, in which the need to acquire food and water and the need to avoid threats are simultaneously integrated into the lives of rats, to examine sex differences in mitigating threat risk while foraging. Rats lived for an extended period (∼2 months) in enlarged chambers that consisted of a safe, bedded nest and a risky foraging area where footshocks could be delivered unpredictably. We observed that male and female rats used different strategies for responding to the threat of footshock. Whereas male rats increased the size of meals consumed to reduce the overall time spent foraging, female rats sacrificed their metabolic needs in order to avoid shocks. Ovarian hormone fluctuations were shown to exert slight but reliable rhythmic effects on risky decision-making in gonadally intact female rats. However, this did not produce significant differences in approach-avoidance trade-offs between ovariectomized and intact female groups, suggesting that male-female sex differences are not due to the activational effects of gonadal hormones but, rather, are likely to be organized during early development.
| S-EPMC5292597 | biostudies-literature
Project description:The effect of sexual selection on extinction risk remains unclear. In theory, sexual selection can lead to both increase and decrease extinction probability depending on the ecology of the study system. Thus, combining different groups might obscure patterns that can be found in groups that share similar ecological features. Using phylogenetic comparative analysis, we studied sexual plumage dimorphism in relation to the perceived risk of extinction in hirundines (subfamily: Hirundininae), in which all species are socially monogamous aerial foragers. Among the 72 species studied, five species are facing a perceived threat of extinction. Species with sexually dimorphic plumage had a higher risk of extinction than did species with sexually monomorphic plumage. Likewise, when focusing solely on tail ornamentation, species that exhibit a sexual dimorphism in tail length had a higher risk of extinction than did other species. In Hirundininae, which are affected a great deal by severe weather, sexual selection and the resultant sexual dimorphism would increase extinction risk.
| S-EPMC5773298 | biostudies-literature
Project description:Males and females generally have different finger proportions. In males, digit 2 is shorter than digit 4, but in females digit 2 is the same length or longer than digit 4. The second- to fourth-digit (2D:4D) ratio correlates with numerous sexually dimorphic behavioral and physiological conditions. Although correlational studies suggest that digit ratios reflect prenatal exposure to androgen, the developmental mechanism underlying sexually dimorphic digit development remains unknown. Here we report that the 2D:4D ratio in mice is controlled by the balance of androgen to estrogen signaling during a narrow window of digit development. Androgen receptor (AR) and estrogen receptor α (ER-α) activity is higher in digit 4 than in digit 2. Inactivation of AR decreases growth of digit 4, which causes a higher 2D:4D ratio, whereas inactivation of ER-α increases growth of digit 4, which leads to a lower 2D:4D ratio. We also show that addition of androgen has the same effect as inactivation of ER and that addition of estrogen mimics the reduction of AR. Androgen and estrogen differentially regulate the network of genes that controls chondrocyte proliferation, leading to differential growth of digit 4 in males and females. These studies identify previously undescribed molecular dimorphisms between male and female limb buds and provide experimental evidence that the digit ratio is a lifelong signature of prenatal hormonal exposure. Our results also suggest that the 2D:4D ratio can serve as an indicator of disrupted endocrine signaling during early development, which may aid in the identification of fetal origins of adult diseases.
| S-EPMC3182741 | biostudies-literature
Project description:Influenza virus transmission between mothers and nursing-infants has not been investigated although mothers and infants often develop severe disease. Ferrets are considered the most appropriate model for influenza studies. We investigated influenza transmission in infant and nursing-mother ferrets. Influenza infected infants transmitted virus to mother mammary glands leading to live virus excretion in milk and influenza virus positive mammary gland epithelial cells. Global gene expression analysis showed down-regulation of milk production and induction of breast involution and oncogenesis pathways. Our results provide insight into influenza transmission between mothers and infants which may impact fields of infectious disease, maternal/infant health and neoplasm etiology. Total RNA was obtained from nursing mother ferret mammary glands at days 3/4 and 6/7 post-intranasal kit infection with 10^5 EID50 A/California/07/2009 (H1N1). Total RNA was also collected from uninfected control nursing mother mammary gland tissues (n = 3). Changes in gene expression relative to uninfected tissue controls were then investigated.
2015-09-10 | E-GEOD-63082 | biostudies-arrayexpress
Project description:Obesity-associated morbidity is exacerbated by abdominal obesity, which can be measured as the waist-to-hip ratio adjusted for the body mass index (WHRadjBMI). Here we identify genes associated with obesity and WHRadjBMI and characterize allele-sensitive enhancers that are predicted to regulate WHRadjBMI genes in women. We found that several waist-to-hip ratio-associated variants map within primate-specific Alu retrotransposons harboring a DNA motif associated with adipocyte differentiation. This suggests that a genetic component of adipose distribution in humans may involve co-option of retrotransposons as adipose enhancers. We evaluated the role of the strongest female WHRadjBMI-associated gene, SNX10, in adipose biology. We determined that it is required for human adipocyte differentiation and function and participates in diet-induced adipose expansion in female mice, but not males. Our data identify genes and regulatory mechanisms that underlie female-specific adipose distribution and mediate metabolic dysfunction in women.
| S-EPMC10375400 | biostudies-literature
Project description:ContextCrosstalk through receptor ligand interactions at the maternal-fetal interface is impacted by fetal sex. This affects placentation in the first trimester and differences in outcomes. Sexually dimorphic signaling at early stages of placentation are not defined.ObjectiveInvestigate the impact of fetal sex on maternal-fetal crosstalk.DesignReceptors/ligands at the maternal-fetal surface were identified from sexually dimorphic genes between fetal sexes in the first trimester placenta and defined in each cell type using single-cell RNA-Sequencing (scRNA-Seq).SettingAcademic institution.SamplesLate first trimester (~10-13 weeks) placenta (fetal) and decidua (maternal) from uncomplicated ongoing pregnancies.Main outcome measuresTranscriptomic profiling at tissue and single-cell level; immunohistochemistry of select proteins.ResultsWe identified 91 sexually dimorphic receptor-ligand pairs across the maternal-fetal interface. We examined fetal sex differences in 5 major cell types (trophoblasts, stromal cells, Hofbauer cells, antigen-presenting cells, and endothelial cells). Ligands from the CC family chemokine ligand (CCL) family were most highly representative in females, with their receptors present on the maternal surface. Sexually dimorphic trophoblast transcripts, Mucin-15 (MUC15) and notum, palmitoleoyl-protein carboxylesterase (NOTUM) were also most highly expressed in syncytiotrophoblasts and extra-villous trophoblasts respectively. Gene Ontology (GO) analysis using sexually dimorphic genes in individual cell types identified cytokine mediated signaling pathways to be most representative in female trophoblasts. Upstream analysis demonstrated TGFB1 and estradiol to affect all cell types, but dihydrotestosterone, produced by the male fetus, was an upstream regulator most significant for the trophoblast population.ConclusionsMaternal-fetal crosstalk exhibits sexual dimorphism during placentation early in gestation.
| S-EPMC7571453 | biostudies-literature
Project description:The molecular mechanisms that control the timing of sexual differentiation in the brain are poorly understood. We found that the timing of sexually dimorphic differentiation of postmitotic, sex-shared neurons in the nervous system of the Caenorhabditis elegans male is controlled by the temporally regulated miRNA let-7 and its target lin-41, a translational regulator. lin-41 acts through lin-29a, an isoform of a conserved Zn finger transcription factor, expressed in a subset of sex-shared neurons only in the male. Ectopic lin-29a is sufficient to impose male-specific features at earlier stages of development and in the opposite sex. The temporal, sexual and spatial specificity of lin-29a expression is controlled intersectionally through the lin-28/let-7/lin-41 heterochronic pathway, sex chromosome configuration and neuron-type-specific terminal selector transcription factors. Two Doublesex-like transcription factors represent additional sex- and neuron-type specific targets of LIN-41 and are regulated in a similar intersectional manner.
| S-EPMC6312707 | biostudies-literature