Deletion of adrenocortical Bmal1 results in sex-biased gene expression.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA532593 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8889300.fastq.gz | Fastqsanger.gz | |||
| SRR8889310.fastq.gz | Fastqsanger.gz | |||
| SRR8889301.fastq.gz | Fastqsanger.gz | |||
| SRR8889311.fastq.gz | Fastqsanger.gz | |||
| SRR8889302.fastq.gz | Fastqsanger.gz |
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Project description:We report that deletion of BMAL1 from adrenocortical cells using a SCC(Cyp11a1)-Cre driver reults in elevated plasma corticosterone in female, but not in male mice, following submaximal stress stimulation. RNA sequencing of adrenal glands from control and experimental animals was adopted to identify sex-dependent differences in gene expression that may explain the augmented corticosterone response specifically in female mice.
2019-04-13 | GSE129725 | GEO
Project description:Investigatation into how genes with sex-differential expression profiles are distributed among the chromosomes in Drosophila. Assayed the expression of 14,142 predicted transcripts in competitive hybridizations and found a dramatic underrepresentation of X-chromosome genes showing high relative expression in male. This is the first report of sex-biased expression of the full (predicted) genome. Findings indicate that there is significant sex-biased expression, especially in gonads. Genes showing sex-biased gene expression profiles are likely to have sex-biased functions. Keywords: other
2003-06-02 | GSE442 | GEO
Project description:The product of the Bmal1 locus is an essential component of the circadian clock that plays important roles in various aspects of reproductive biology, and its disruption results in infertility. In an effort to identify the identity of the tissue specific clock that is responsible for this infertility, we used the steroidogenic factor-1 (Sf1) promoter to drive Cre-mediated recombination and genetically delete Bmal1 within cells of the reproductive axis. We show that Bmal1 within the reproductive axis of females is essential for normal fertility through its role in maintaining implantation, but is not required for normal estrous cycling. At the root of this biology appears to be a defect in the regulation of ovarian steroidogenic acute regulator (StAR) and its role in maintaining progesterone synthesis. This conclusion is based upon three observations. First, that deletion of Bmal1 within the reproductive axis leads to lower levels of StAR mRNA, and lower progesterone levels. Second, that progesterone supplementation of these conditional mutants rescues implantation. Third, transplantation of wild type ovaries into Bmal1 reproductive axis mutants results in 100% fertility. Our study suggests that ovarian Bmal1 is an essential peripheral clock governing implantation and fertility in female mice. Ten week old female Bmal1fxfx mice positive or negative for Cre-recombinase driven by the sf-1 promoter, housed in 12 hour light:12 dark, ad lib feeding and drinking conditions were sacrificed at ZT12 on 3.5dpc (3.5 days post copulation). For each array analysis, a pool of 3 RNA samples from 3 individual Bmal1fx/fxCresf-1 ovaries labeled with cy3 were co-hybridized with a pool of 3 RNA samples from Bmal1fx/fx ovaries labeled with cy5, according to Agilent protocols.
2013-02-01 | E-GEOD-38365 | biostudies-arrayexpress
Project description:The product of the Bmal1 locus is an essential component of the circadian clock that plays important roles in various aspects of reproductive biology,and when disrupted results in infertility. In an effort to establish the identity of the tissue specific clock that is responsible for this infertility, we used the steroidogenic factor-1 (Sf1) promoter to drive Cre-mediated recombination and genetically delete Bmal1 within cells of the reproductive axis. We show that Bmal1 within the reproductive axis of females is essential for normal fertility through its role in maintaining implantation, but is not required for normal estrous cycling. At the root of this biology appears to be a defect in the ovaries, including regulation of ovarian lipid biosynthetic or metabolic processes and their roles in maintaining progesterone synthesis. This conclusion is based upon three observations. First, that deletion of Bmal1 within the reproductive axis reducesleads to affected transcripts in steroidogenic pathways for the LH receptor , and lowers progesterone levels. Second, that progesterone supplementation of these conditional mutants rescues implantation. Third, transplantation of wild type ovaries into Bmal1 reproductive axis mutants rescues fertility. Our study demonstrates the significance of ovarian Bmal1 as an overriding influence in experimental models of infertility. A time series was performed in time-mated C57Bl/6J mice to identiy oscillating transcripts. During the peak and trough of the majority of transcripts (ZT0 and ZT12) samples from Bmal1fx/fx Sf1Cre mice and control litermates as well and global Bmal1 nulls were also analyzed. The tissue types (ovary, pituitary) are not comparable.
2014-10-01 | E-GEOD-48758 | biostudies-arrayexpress
Project description:The product of the Bmal1 locus is an essential component of the circadian clock that plays important roles in various aspects of reproductive biology, and its disruption results in infertility. In an effort to identify the identity of the tissue specific clock that is responsible for this infertility, we used the steroidogenic factor-1 (Sf1) promoter to drive Cre-mediated recombination and genetically delete Bmal1 within cells of the reproductive axis. We show that Bmal1 within the reproductive axis of females is essential for normal fertility through its role in maintaining implantation, but is not required for normal estrous cycling. At the root of this biology appears to be a defect in the regulation of ovarian steroidogenic acute regulator (StAR) and its role in maintaining progesterone synthesis. This conclusion is based upon three observations. First, that deletion of Bmal1 within the reproductive axis leads to lower levels of StAR mRNA, and lower progesterone levels. Second, that progesterone supplementation of these conditional mutants rescues implantation. Third, transplantation of wild type ovaries into Bmal1 reproductive axis mutants results in 100% fertility. Our study suggests that ovarian Bmal1 is an essential peripheral clock governing implantation and fertility in female mice.
2013-02-01 | GSE38365 | GEO
Project description:Background: Stalk-eyed flies (family Diopsidae) are a model system for studying sexual selection due to the presence of elongated and sexually dimorphic eye-stalks in many species. Recent genomic studies on these flies have revealed a neo-X chromosome and evidence of gene movement onto or off of this X chromosome. To determine if sex linkage and gene movement are related to sexual dimorphism and sexual conflict, we compared gene expression between males and females using oligonucleotide microarrays and RNA from either developing eyestalk tissue or adult heads from a dimorphic species, Teleopsis dalmanni, or from developing eyestalk tissue in a congeneric monomorphic species, T. quinqueguttata. Results: Comparison of gene expression between the sexes for 3,748 genes indicates that dosage compensation is present due to elevated expression of X-linked genes in males. However, sex-biased expression was detected in 26% of the genes present in eye-antennal imaginal discs of larval T. dalmanni. Functional annotation reveals that female-biased genes are associated with transcription, anatomical development and cell communication in the nucleus, while male-biased genes are associated with metabolism and the mitochondria. Comparison of gene expression between experiments identified 140 genes with concordant sex-biased expression in the larval and adult tissues of T. dalmanni and 17 genes with identical sex-biased expression between species. There were only five reversals of sex-biased expression across experiments. In T. dalmanni, male-biased genes are more common on autosomes than on the X while female-biased genes are more common on the X in T. quinqueguttata. Female-biased expression is especially common among genes that moved onto the ancestral X while male-biased expression is more common among genes that moved onto an autosome. Conclusions: Genes with sex-biased expression exhibit different functions in each sex as expected if sexual conflict has influenced their evolution. The strong relationship between sex-biased expression and gene movement found in this study is consistent with resolution of sexual conflict by an RNA- or DNA-mediated process that moves genes between chromosomes. Measurement of gene expression in additional species should provide a more complete picture of how gene expression change occurs over evolutionary time in these extraordinary flies. Two-condition experiment, female vs. male RNA using larval eye discs for two species (Teleopsis dalmanni, Teleopsis quinqueguttata), and adult heads for one species (Teleopsis dalmanni).
2012-04-09 | E-GEOD-37121 | biostudies-arrayexpress
Project description:The product of the Bmal1 locus is an essential component of the circadian clock that plays important roles in various aspects of reproductive biology,and when disrupted results in infertility. In an effort to establish the identity of the tissue specific clock that is responsible for this infertility, we used the steroidogenic factor-1 (Sf1) promoter to drive Cre-mediated recombination and genetically delete Bmal1 within cells of the reproductive axis. We show that Bmal1 within the reproductive axis of females is essential for normal fertility through its role in maintaining implantation, but is not required for normal estrous cycling. At the root of this biology appears to be a defect in the ovaries, including regulation of ovarian lipid biosynthetic or metabolic processes and their roles in maintaining progesterone synthesis. This conclusion is based upon three observations. First, that deletion of Bmal1 within the reproductive axis reducesleads to affected transcripts in steroidogenic pathways for the LH receptor , and lowers progesterone levels. Second, that progesterone supplementation of these conditional mutants rescues implantation. Third, transplantation of wild type ovaries into Bmal1 reproductive axis mutants rescues fertility. Our study demonstrates the significance of ovarian Bmal1 as an overriding influence in experimental models of infertility.
2014-10-01 | GSE48758 | GEO
Project description:Purpose: Accurate identification of sex-biased genes requires precise measurement of gene expression levels in gonads. This study is designed to provide such data for various Drosophila species to enhance studies of sex-biased gene expression and evolution across the genus. Methods: Virgin flies were collected and aged 6-10 days before dissecting 2-3 replicates of testes or ovaries. Total RNA was extracted using the Arcturus® PicoPure® kit . Illumina® TruSeq® RNA library kits were used to poly-A+ select and reverse-transcribe mRNA, shear cDNA into ~120 bp fragments, and produce libraries for 1x50 bp sequencing on an Illumina GAIIx or HiSeq2000. Illumina®’s Real Time Analysis v1.13 module processed images, called bases, and provided base qualities. Reads were mapped to the current reference genomes using Bowtie v2.1.0 (Langmead and Salzberg, 2012, Nat Meth) with default settings. Differentially expressed genes were detected using Cufflinks v 2.1.0 (Trapnell et al., 2010, Nat Biotech; default settings) or edgeR (Robinson et al., 2010, Bioinformatics; full-quantile GC-content normalization and full-quantile between-sample normalization). Genes were called differentially expressed at a Benjamini-Hochberg false discovery rate of 0.01. Results: Thousands of male- and female-biased genes were detected for each species using both DE detection methods. These results provide a significant improvement in sensitivity of sex-biased gene detection relative to using whole-body RNA-sequencing data. These data provide a foundation for accurate identification of sex-biased genes throughout the Drosophila genus. Testis and ovary samples from Drosophila species were sequenced 1 x 50 bp in duplicate from 6-10 day old virgin, Wolbachia-free adult flies on an Illumina GAIIx or HiSeq2000.
2013-11-04 | E-GEOD-52058 | biostudies-arrayexpress
Project description:Circadian rhythm dysfunction is a hallmark of Parkinson Disease (PD), and diminished expression of the core clock gene Bmal1 has been described in PD patients. BMAL1 is required for core circadian clock function, but also serves non-rhythmic functions. Germline Bmal1 deletion can cause brain oxidative stress and synapse loss in mice, and can exacerbate dopaminergic neurodegeneration in response to MPTP. Here we examined the impact of cell type-specific Bmal1 deletion on dopaminergic neuron viability in vivo. We observed that global, post-natal deletion of Bmal1 caused spontaneous loss of tyrosine hydroxylase-positive (TH+) dopaminergic neurons in the substantia nigra pars compacta (SNpc). This was not due to disruption of behavioral circadian rhythms, and was not induced by astrocyte- or microglia-specific Bmal1 deletion. However, either pan-neuronal or TH neuron-specific Bmal1 deletion caused cell-autonomous loss of TH+ neurons in the SNpc. Finally, global Bmal1 deletion exacerbated TH+ neuron loss following injection of alpha-synclein fibrils. Transcriptomic analysis of neuron-specific Bmal1 KO brain revealed dysregulation of pathways involved in oxidative phosphorylation and Parkinson Disease.
2023-08-18 | GSE241200 | GEO
Project description:The difference in X chromosome copy number creates a potential difference in X chromosomal gene expression between males and females. In many animals, dosage compensation mechanisms equalize X chromosome expression between sexes. Yet, X chromosome is also enriched for sex-biased genes due to differences in the evolutionary history of the X and autosomes. The manner in which dosage compensation and sex-biased gene expression exist on the X chromosome remains an open question. Most studies compare gene expression between two sexes, which combines expression differences due to X chromosome number (dose) and sex. Here, we uncoupled the effects of sex and X dose in C. elegans and determined how each process affects expression of the X chromosome compared to autosomes. We found that in the soma, sex-biased expression on the X chromosome is almost entirely due to sex because the dosage compensation complex (DCC) effectively compensates for the X dose difference between sexes. In the germline where the DCC is not present, X chromosome copy number contributes to hermaphrodite-biased gene expression. These results suggest that X dose contributes to sex-biased gene expression based on the level of dosage compensation in different tissues and developmental stages. RNA-Seq profiles of C. elegans XO hermaphrodite and XX male L3 larvae and adults
2016-04-06 | E-GEOD-77794 | biostudies-arrayexpress