Modulation by NPYR underlies experience-dependent, sexually dimorphic learning
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ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE273091 | GEO | 2024/07/25
REPOSITORIES: GEO
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Project description:Many species undergo sexual reproduction to distribute the parental genomes and increase the genomic diversity of the progeny. Among such species, sexual dimorphism is often displayed through morphology, size, behavior, and life-span, depending on the survival and reproduction strategies of the species. The nematode Caenorhabditis elegans has two sexes, hermaphrodite and male, and only the hermaphrodites, which produce both oocytes and sperm, are essential for the perpetuation of the species. In this study, we found that dietary restriction, which is the most reproducible way to retard aging in many species, extends the life-span of C. elegans hermaphrodites but not that of males. Our analysis revealed that fasting induces male-enriched genes in hermaphrodites and that the sex determination pathway affects life-span regulation, even after the completion of development, and is regulated by food availability. Furthermore, fasting activates the entire X-chromosome only in hermaphrodites. Our tiling array analysis identified a fasting-inducible, X-linked non-coding RNA for which expression positively correlated with the activation level of the X-chromosome and longevity. These links between the sex determination mechanism and dietary restriction at multiple levels may give priority to the survival of hermaphrodites during food shortages in C. elegans.
2017-12-07 | GSE37303 | GEO
Project description:Despite sharing much of their genomes, males and females are often highly dimorphic, reflecting at least in part the resolution of sexual conflict in response to sexually antagonistic selection. Sexual dimorphism arises owing to sex differences in gene expression, and steroid hormones are often invoked as a proximate cause of sexual dimorphism. Experimental elevation of androgens can lead to masculinization of behavior, physiology, and gene expression, but knowledge of the role of hormones remains incomplete, including how the sexes differ in their gene expression in response to exposure to hormones. We addressed these questions in a bird species with a long history of behavioral endocrinological and ecological study, the dark-eyed junco (Junco hyemalis), using a species-specific microarray. Focusing on two brain regions involved in sexually dimorphic behavior and regulation of hormone secretion, we identified 1,639 genes that differed in expression by sex in the ventromedial telencephalon and 768 in hypothalamus. In response to experimentally elevated testosterone, females exhibited a more “male-like” expression pattern than control females; unexpectedly, male expression patterns became more “female-like” rather than hyper-masculinized when compared to control males. This sex difference in pattern arose both because testosterone altered regulation of different genes in each sex and because testosterone altered regulation of the same genes differentially, i.e., up in one sex, down in the other. Hormonally regulated gene expression is a key genetic and physiological mechanism underlying sexual dimorphism, and further study should help to explain how it relates to the resolution of sexual conflict. Hypothalamus: 24 samples were analyzed, all were biological (not technical) replicates. 6 from males treated with testosterone [MT], 6 from control males [MC], 6 from females treated with testosterone [FT], and 6 from control females [FC]. All hybridizations were paired, and all treatment groups were compared, but no sample was analyzed more than once. Ventromedial telencephalon: 24 samples were analyzed, all were biological (not technical) replicates. 6 from males treated with testosterone [MT], 6 from control males [MC], 6 from females treated with testosterone [FT], and 6 from control females [FC]. All hybridizations were paired, and all treatment groups were compared, but no sample was analyzed more than once.
2013-01-30 | E-GEOD-41076 | biostudies-arrayexpress
Project description:SMC3 is a chromatin binding factor that plays central roles in genome organization and in proper neurodevelopment. Mutations in SMC3 gene (SMC3) induce neurodevelopmental and behavioral phenotypes in humans, including changes in anxiety behavior and self-injury. However, it is not clear what are the exact roles of SMC3 in behavior in adulthood or if its effects are only developmental. Using an adulthood forebrain excitatory neuron specific Smc3 knockout mouse model, the current study determined specific sex-dependent effects of SMC3 ablation during the adulthood. Behavioral tests identified anxiolytic effects of Smc3 knockout in females and anxiogenic effects in males four weeks after initiation of adulthood knockout. The prefrontal cortex, a regulator of anxiety behavior, also displayed sex-dependent effects in dendritic complexity. Transcriptional analysis revealed differential effects of Smc3 knockout in males and females, including changes in anxiety-related genes and relevant transcriptional pathways. While anxiety behavior was sex-specific, both males and females developed self-injury behavior at approximately ten weeks after induction of knockout. The current study demonstrates that neuronal SMC3 regulates anxiety during the adulthood in a sex-specific manner.
2024-09-01 | GSE270835 | GEO
Project description:Fragile X Syndrome is an inherited X-linked disorder associated with intellectual disabilities that begin in childhood and last a lifetime. The symptoms overlap with autism spectrum disorder, and the syndrome predominantly affects males. Consequently, FXS research tends to favor analysis of social behaviors in males, leaving a gap in our understanding of other behavioral traits, especially in females. Here we used a mouse model of FXS to analyze developmental, behavioral, neurochemical, and transcriptomic profiles in males and females. Our behavioral assays demonstrated locomotor hyperactivity, motor impulsivity, increased “approach” behavior in an approach-avoidance assay, and deficits in nest building behavior. Analysis of brain neurotransmitter content revealed deficits in striatal GABA, glutamate, and serotonin content. RNA sequencing of the ventral striatum unveiled expression changes associated with neurotransmission as well as motivation and substance use pathways. Sex differences were identified in nest building behavior, striatal neurotransmitter content, and ventral striatal gene expression. In summary, our study identified sex differences in specific behavioral, neurotransmitter, and gene expression phenotypes and gene set enrichment analysis identified significant enrichment of pathways associated with motivation and drug reward.
2024-08-26 | GSE275170 | GEO
Project description:The nematode Auanema rhodensis is trioecious (co-occurrence of males, females and self-fertile hermaphrodites). To better understand its sex determination system, we have compared the transcriptomic profiles of early (L2) females, hermaphrodites and converted females (hermaphrodite-fated larvae induced to develop as females). Additionally, we sequenced the transcriptome of adult males and individuals from various stages and sexes (mixed stages samples) to compare global gene expression profiles along the assembled draft chromosomes of A. rhodensis (BioProject PRJEB29492). The RNA-seq data was also used to predict genes in the assembled genome. We generated three biological replicates for each RNA-seq condition (L2 females, L2 converted females, L2 hermaphrodites, males and mixed stages). Comparisons of the expression profiles of the L2 conditions was performed to identify genes potentially involved in the sexual differentiation process, using a standard RNA-seq comparison approach. Briefly, the cleaned reads were aligned to the genome using STAR, the abundance and identification of differentially expressed genes were assessed using FeatureCounts and DEseq2 (using as thresholds an absolute log2(Fold Change) >= 2 and an FDR <0.01).
2019-02-11 | E-MTAB-7667 | biostudies-arrayexpress
Project description:Neuroligin-4 (NL4) loss-of-function mutations are strongly associated with monogenic heritable abnormalities linked with Autism Spectrum Disorder (ASD). NL4 mutation in mice causes ASD related alterations in both, the synaptic and behavioral phenotype. Since microglia closely regulate synaptic development and are implicated as key players in ASD development and progression, we here studied microglial properties in the NL4-/- mouse model. We show that loss of NL4 caused altered behavior and impaired hippocampal gamma oscillations predominantly in male mice. In parallel, microglial density, morphology, and response to injury specifically in the CA3 region of the hippocampus were altered in NL4-deficient males only. A transcriptomic and proteomic analysis revealed a strong impact of sexual dimorphism on molecular alterations in microglia of NL4-deficient compared to wildtype mice. Estrogen application in male NL4-/- animals partially restored the impaired social behavior and the altered microglial phenotype. Together, these results indicate that loss of NL4 affects not only neuronal network activity and behavior, but changes in addition the phenotype of microglia in a sex-specific manner that could be targeted by estrogen treatment.
2023-10-24 | PXD024325 | Pride
Project description:Despite sharing much of their genomes, males and females are often highly dimorphic, reflecting at least in part the resolution of sexual conflict in response to sexually antagonistic selection. Sexual dimorphism arises owing to sex differences in gene expression, and steroid hormones are often invoked as a proximate cause of sexual dimorphism. Experimental elevation of androgens can lead to masculinization of behavior, physiology, and gene expression, but knowledge of the role of hormones remains incomplete, including how the sexes differ in their gene expression in response to exposure to hormones. We addressed these questions in a bird species with a long history of behavioral endocrinological and ecological study, the dark-eyed junco (Junco hyemalis), using a species-specific microarray. Focusing on two brain regions involved in sexually dimorphic behavior and regulation of hormone secretion, we identified 1,639 genes that differed in expression by sex in the ventromedial telencephalon and 768 in hypothalamus. In response to experimentally elevated testosterone, females exhibited a more “male-like” expression pattern than control females; unexpectedly, male expression patterns became more “female-like” rather than hyper-masculinized when compared to control males. This sex difference in pattern arose both because testosterone altered regulation of different genes in each sex and because testosterone altered regulation of the same genes differentially, i.e., up in one sex, down in the other. Hormonally regulated gene expression is a key genetic and physiological mechanism underlying sexual dimorphism, and further study should help to explain how it relates to the resolution of sexual conflict. Males and females can be highly dimorphic in metabolism and physiology despite sharing nearly identical genomes, and males and females both respond phenotypically to elevated testosterone, a steroid hormone that alters gene expression. Only recently has it become possible to learn how a hormone like testosterone affects global gene expression in non-model systems, and whether it affects the same genes in males and females. To investigate the transcriptional mechanisms by which testosterone exerts its metabolic and physiological effects on the periphery, we compared gene expression by sex and in response to experimentally elevated testosterone in a well-studied bird species, the dark-eyed junco (Junco hyemalis). We identified 324 genes in the liver, and 733 in the pectoralis muscle that were differentially expressed between males and females. In addition, we identified 1,872 genes that were differentially expressed between testosterone-treated and control individuals in at least one tissue and sex. Testosterone-treatment altered the expression of only130 genes in both males and females in the same tissue. These substantial differences in transcriptional response to testosterone suggest that males and females may employ different pathways when responding to elevated testosterone, despite the fact that many phenotypic effects of experimentally elevated testosterone are similar in the sexes. In contrast, of the 130 genes that were affected by testosterone-treatment in both sexes, 78% were regulated in the same direction (e.g. either higher or lower in testosterone-treated than control males and females). Thus, it appears that testosterone acts through both unique and shared transcriptional pathways in males and females, suggesting multiple mechanisms by which sexual conflict can be mediated.
2013-01-30 | GSE41076 | GEO
Project description:Objective: Sexually dimorphic phenotypes arise largely from sex-specific gene expression, which has mainly been characterized in sexually naïve adults. However, we expect sexual dimorphism in transcription to be dynamic and dependent on factors such as reproductive status. Mating induces many behavioral and physiological changes distinct to each sex and is therefore expected to activate regulatory changes in many sex-biased genes. Methods: Using RNA-seq we first characterized sexual dimorphism in gene expression, for the first time in Callosobruchus maculatus seed beetles. We then examined how females and males respond to mating and how it affects sex-biased expression, both in more sex-limited (abdomen) and sex-shared (head and thorax) tissues. Results: Mating responses were largely sex-specific and, as expected, females showed more numerous changes compared to males. Of the sex-biased genes present in virgins, 16% (1,041 genes) in the abdomen and 17% (243 genes) in the head and thorax altered their relative expression between the sexes. Sex-bias status changed in 2% of the genes in the abdomen and 4% in the head and thorax following mating. Mating responses involved de-feminization of females and, to a lesser extent, de-masculinization of males relative to their virgin state: mating decreased rather than increased dimorphic expression of sex-biased genes.
2016-12-23 | GSE92855 | GEO
Project description:The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. Two-channel experiment comparing mixed stage sample to mixed stage mixed 50:50 N2,CB4856 common reference
2013-07-30 | E-GEOD-49307 | biostudies-arrayexpress
Project description:Schistosoma mansoni is a dioecious species, that is, it has two differentiated sexes. Interestingly, this sexual species evolved from a hermaphrodite ancestor. Indeed, most Platyhelminthes are hermaphrodites. Here we characterize the microRNAs of S. mansoni and quantify their differential expression between males and females.
2013-07-31 | GSE49359 | GEO