Deciphering the Developmental Dynamics of the Mouse Liver Transcriptome
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE58827 | GEO | 2014/10/16
SECONDARY ACCESSION(S): PRJNA253659
REPOSITORIES: GEO
Similar Datasets
Project description:This study uses Whole Transcriptome Shotgun Sequencing (RNA-Seq) data to interrogate the developmental dynamics of the C57BL/6 mouse liver transcriptome. We analyze gene expression patterns in the developing mouse liver over 12 distinct time points from late embryonic stage (2 days before birth) to maturity (60 days after birth). Biological functions deemed significant at different developmental stages are identified and their leverage is mapped over time. Upstream regulators modulating these gene expression patterns are determined and their regulatory networks are described along with putative transcriptional modules associated with gene regulation. Several genes that were alternatively spliced over time were identified. Previously uncharacterized isoforms were found for several genes. We analyze gene expression patterns in the developing mouse liver over 12 distinct time points from late embryonic stage (2 days before birth) to maturity (60 days after birth). Three replicates per time point.
2014-10-16 | E-GEOD-58827 | biostudies-arrayexpress
Project description:Inborn errors of lipid metabolism illustrate the importance of proper milk fat oxidation in newborn mammals. In the liver, a remarkable lipid catabolic competence is present at birth; however, it is unclear how this critical trait is acquired and regulated. In this work, we found that the genes required for milk lipid catabolism are already transcribed before birth in the term fetus (E19.5) and controlled by the peroxisome-proliferator activated receptor alpha (PPARα) in mouse liver. The developmental activity of PPARα strongly regulates fatty acid oxidation genes. Two days after birth (P2), during milk suckling, PPARα-null mice develop a congenital steatosis and milk protein oxidation is de-repressed to fuel an alternative energy pathway that maintains glucose homeostasis and postnatal growth. Our results demonstrate for the first time, the developmental role of PPARα in regulating the metabolic ability to use maternal milk as fuel in the early days of life.
2016-06-01 | GSE39670 | GEO
Project description:Inborn errors of lipid metabolism illustrate the importance of proper milk fat oxidation in newborn mammals. In the liver, a remarkable lipid catabolic competence is present at birth; however, it is unclear how this critical trait is acquired and regulated. In this work, we found that the genes required for milk lipid catabolism are already transcribed before birth in the term fetus (E19.5) and controlled by the peroxisome-proliferator activated receptor alpha (PPARα) in mouse liver. The developmental activity of PPARα strongly regulates fatty acid oxidation genes. Two days after birth (P2), during milk suckling, PPARα-null mice develop a congenital steatosis and milk protein oxidation is de-repressed to fuel an alternative energy pathway that maintains glucose homeostasis and postnatal growth. Our results demonstrate for the first time, the developmental role of PPARα in regulating the metabolic ability to use maternal milk as fuel in the early days of life.
2016-06-01 | GSE39669 | GEO
Project description:Inborn errors of lipid metabolism illustrate the importance of proper milk fat oxidation in newborn mammals. In the liver, a remarkable lipid catabolic competence is present at birth; however, it is unclear how this critical trait is acquired and regulated. In this work, we found that the genes required for milk lipid catabolism are already transcribed before birth in the term fetus (E19.5) and controlled by the peroxisome-proliferator activated receptor alpha (PPARα) in mouse liver. The developmental activity of PPARα strongly regulates fatty acid oxidation genes. Two days after birth (P2), during milk suckling, PPARα-null mice develop a congenital steatosis and milk protein oxidation is de-repressed to fuel an alternative energy pathway that maintains glucose homeostasis and postnatal growth. Our results demonstrate for the first time, the developmental role of PPARα in regulating the metabolic ability to use maternal milk as fuel in the early days of life. Expression profile difference between PPARalpha wild-type (3 males and 3 females) and knock-out (3 males and 3 females) mouse liver in suckling mice. Two days after birth, pups were killed and their liver promptly removed and frozen in liquid nitrogen.
2016-06-01 | E-GEOD-39670 | biostudies-arrayexpress
Project description:The liver performs a number of essential functions for life. The development of such a complex organ relies on finely regulated gene expression profiles which change over time in the development and determine the phenotype and function of the liver. We used high-density oligonucleotide microarrays to study the gene expression and transcription regulation at 14 time points across the C57/B6 mouse liver development, which include E11.5 (embryonic day 11.5), E12.5, E13.5, E14.5, E15.5, E16.5, E17.5, E18.5, Day0 (the day of birth), Day3, Day7, Day14, Day21, and normal adult liver. With these data, we made a comprehensive analysis on gene expression patterns, functional preferences and transcriptional regulations during the liver development. Keywords: time course
2008-10-30 | GSE13149 | GEO
Project description:Inborn errors of lipid metabolism illustrate the importance of proper milk fat oxidation in newborn mammals. In the liver, a remarkable lipid catabolic competence is present at birth; however, it is unclear how this critical trait is acquired and regulated. In this work, we found that the genes required for milk lipid catabolism are already transcribed before birth in the term fetus (E19.5) and controlled by the peroxisome-proliferator activated receptor alpha (PPARα) in mouse liver. The developmental activity of PPARα strongly regulates fatty acid oxidation genes. Two days after birth (P2), during milk suckling, PPARα-null mice develop a congenital steatosis and milk protein oxidation is de-repressed to fuel an alternative energy pathway that maintains glucose homeostasis and postnatal growth. Our results demonstrate for the first time, the developmental role of PPARα in regulating the metabolic ability to use maternal milk as fuel in the early days of life. Expression profile difference between PPARalpha wild-type (n=6) and knock-out (n=6) mouse liver at fetal day E19.5. Term fetuses were collected by cesarean section, their liver promptly dissected and frozen in liquid nitrogen.
2016-06-01 | E-GEOD-39669 | biostudies-arrayexpress
Project description:The liver performs a number of essential functions for life. The development of such a complex organ relies on finely regulated gene expression profiles which change over time in the development and determine the phenotype and function of the liver. We used high-density oligonucleotide microarrays to study the gene expression and transcription regulation at 14 time points across the C57/B6 mouse liver development, which include E11.5 (embryonic day 11.5), E12.5, E13.5, E14.5, E15.5, E16.5, E17.5, E18.5, Day0 (the day of birth), Day3, Day7, Day14, Day21, and normal adult liver. With these data, we made a comprehensive analysis on gene expression patterns, functional preferences and transcriptional regulations during the liver development. Experiment Overall Design: Totally 25 microarrays have been used in this experiment, and 11 of the 14 time points have two technique repeat experiments.
2008-11-13 | E-GEOD-13149 | biostudies-arrayexpress
Project description:Expression data from Sheep longissimus dorsi (LD) muscle during development; fetal lambs (80, 100, 120 days gestation), new born lambs at birth (150 d) and lambs at 12 weeks (230 d) The fetal to neonatal developmental transition corresponds with profound changes in skeletal muscle function as it adapts to the new physiological demands of locomotion and postural support against gravity. The mechanisms underpinning this adaption process are unclear but are likely to be initiated by changes in hormone levels occurring during the major developmental transition. We tested the hypothesis that this period is associated with changes in the transcription of skeletal muscle genes, particularly genes involved in oxidative metabolism. Using an ovine model, transcriptional profiling was performed on longissimus dorsi skeletal muscle taken at three fetal developmental time points (80, 100 and 120 d of fetal development) as well as two postnatal time points, one within 3 days after birth and a second at 12 weeks of age. The developmental time course was dominated by large changes in the expression of 2471 genes during the period from late fetal development (120 d fetal development) to birth (within 1-3 days of birth). Analysis of the functions of the genes that were uniquely up-regulated in this period showed strong enrichment for oxidative metabolism and the TCA cycle indicating enhanced mitochondrial activity. Indeed, histological examination of tissues from these developmental time points directly demonstrated a marked increase in mitochondrial activity between the late fetal and early post-natal samples. The genes that were down-regulated in this period suggested de-emphasis of an array of biological functions including Wnt signaling, cell adhesion and differentiation. There were also changes in the expression of genes prior to this late fetal – postnatal transition and between the two postnatal time points that involved a variety of biological functions. It is concluded that there is substantial and coordinated changes in the transcription of a large number of genes in skeletal muscle which underpin the adaption of muscle to the new physiological demands in the postnatal environment. Microarrays were used for transcription profiling of skeletal muscle samples taken from fetal lambs (80, 100, 120 days gestation), new born lambs at birth (150 d) and lambs at 12 weeks (230 d)
2010-06-01 | GSE20112 | GEO
Project description:Subtypes of neocortical projection neurons over developmental time
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Project description:DNA methylation marks are thought to be set up during early development and to remain static thereafter in healthy tissues. Here, we characterize the liver DNA methylation patterns of mice before birth, during early postnatal development (from birth until weaning) and in adulthood. Our analyses show extensive epigenetic reprogramming in the liver occurring during postnatal development. 118,877 of 261,317 CpGs analyzed throughout the genome significantly changed their methylation level by more than 5% from birth to nine weeks of age, with some changing by up to 86%. Interestingly, changes in DNA methylation occur primarily in intergenic enhancer regions while gene promoters seem little affected. Analysis of 166 CpGs at multiple time points by locus-specific bisulfite sequencing reveals that this reprogramming primarily occurs between postnatal day 1 and day 20. This time period coincides with two major cellular changes in the liver: the differentiation of hepatocytes and extensive cell division. While cell multiplication leaves a distinct footprint on the DNA methylation patterns, we show that the extensive epigenetic reprogramming likely results from differentiation of hepatoblasts into hepatocytes. Overall, our data suggest that epigenetic remodeling is an important aspect of normal liver maturation and involves a large number of gene enhancers.
2017-02-08 | GSE79775 | GEO