Affymetrix SNP array data for beak deformity and normal Beijing-You Chickens
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ABSTRACT:
ORGANISM(S): Gallus gallus
PROVIDER: GSE101703 | GEO | 2017/07/21
SECONDARY ACCESSION(S): PRJNA395229
REPOSITORIES: GEO
Similar Datasets
Project description:Avian beaks show extreme species-specific variability in morphology, though they develop from the same primordial structures. In both humans and birds, cranial neural crest cells are the primary source of mesenchyme for the frontonasal prominence; previous work has shown that these cells contain molecular information that regulate species-specific facial variation. To determine the molecular basis of avian craniofacial patterning, we have used Next-Generation sequencing to profile all 20-40nt microRNAs from micro-dissected cranial neural crest cells from the frontonasal prominence of three bird species (chickens, quails, and ducks). Samples for each species were isolated at two developmental stages, before (Hamilton Hamburger stage [HH] 20) and after (HH25) morphological distinctions between the species are evident.
2012-05-02 | GSE30716 | GEO
Project description:Avian beaks show extreme species-specific variability in morphology, though they develop from the same primordial structures. In both humans and birds, cranial neural crest cells are the primary source of mesenchyme for the frontonasal prominence; previous work has shown that these cells contain molecular information that regulate species-specific facial variation. To determine the molecular basis of avian craniofacial patterning, we have used Next-Generation sequencing to profile all 20-40nt microRNAs from micro-dissected cranial neural crest cells from the frontonasal prominence of three bird species (chickens, quails, and ducks). Samples for each species were isolated at two developmental stages, before (Hamilton Hamburger stage [HH] 20) and after (HH25) morphological distinctions between the species are evident. Examination of microRNA expression in frontonasal neural crest cells of 3 bird species at two developmental stages. Includes some biological replicates and one technical replicate.
2012-05-02 | E-GEOD-30716 | biostudies-arrayexpress
Project description:Bipolar disorder (BD) and obesity are highly comorbid. We previously performed a genome-wide association study (GWAS) for BD risk accounting for the effect of body mass index (BMI) which identified a genome-wide significant single-nucleotide polymorphism (SNP) in the gene encoding the transcription factor 7 like 2 (TCF7L2). However, the molecular function of TCF7L2 in the central nervous system (CNS) and its possible role in BD and BMI interaction remained unclear. In the present study, we demonstrated by studying human induced pluripotent stem cell (hiPSC)-derived astrocytes, cells which highly express TCF7L2 in the CNS, that the BD-BMI GWAS risk SNP is associated with glucocorticoid-dependent repression of the expression of a previously uncharacterized TCF7L2 transcript variant. That transcript is a long non-coding RNA (lncRNA-TCF7L2) that is highly expressed in the CNS but not in peripheral tissues such as the liver and pancreas which are involved in metabolism. In astrocytes, knock-down of the lncRNA-TCF7L2 resulted in decreased expression of the parent gene, TCF7L2, as well as alterations in the expression of a series of genes involved in insulin signaling and diabetes. We also studied the function of TCF7L2 in hiPSC-derived astrocytes by integrating RNA sequencing data after TCF7L2 knock-down with TCF7L2 chromatin-immunoprecipitation sequencing (ChIP-seq) data. Those studies showed that TCF7L2 directly regulated a series of BD-risk genes. In summary, these results support the existence of a CNS-based mechanism underlying BD-BMI genetic risk, a mechanism based on a glucocorticoid-dependent expression quantitative trait locus that regulates the expression of a novel TCF7L2 non-coding transcript.
2021-07-21 | GSE179921 | GEO
Project description:Bipolar disorder (BD) and obesity are highly comorbid. We previously performed a genome-wide association study (GWAS) for BD risk accounting for the effect of body mass index (BMI) which identified a genome-wide significant single-nucleotide polymorphism (SNP) in the gene encoding the transcription factor 7 like 2 (TCF7L2). However, the molecular function of TCF7L2 in the central nervous system (CNS) and its possible role in BD and BMI interaction remained unclear. In the present study, we demonstrated by studying human induced pluripotent stem cell (hiPSC)-derived astrocytes, cells which highly express TCF7L2 in the CNS, that the BD-BMI GWAS risk SNP is associated with glucocorticoid-dependent repression of the expression of a previously uncharacterized TCF7L2 transcript variant. That transcript is a long non-coding RNA (lncRNA-TCF7L2) that is highly expressed in the CNS but not in peripheral tissues such as the liver and pancreas which are involved in metabolism. In astrocytes, knock-down of the lncRNA-TCF7L2 resulted in decreased expression of the parent gene, TCF7L2, as well as alterations in the expression of a series of genes involved in insulin signaling and diabetes. We also studied the function of TCF7L2 in hiPSC-derived astrocytes by integrating RNA sequencing data after TCF7L2 knock-down with TCF7L2 chromatin-immunoprecipitation sequencing (ChIP-seq) data. Those studies showed that TCF7L2 directly regulated a series of BD-risk genes. In summary, these results support the existence of a CNS-based mechanism underlying BD-BMI genetic risk, a mechanism based on a glucocorticoid-dependent expression quantitative trait locus that regulates the expression of a novel TCF7L2 non-coding transcript.
2021-07-21 | GSE179762 | GEO
Project description:Goal: To identify copy number variation in normal individuals using high density, non-polymorphic oligonucleotide probes Background DNA sequence diversity within the human genome may be more greatly affected by copy number variations (CNVs) than single nucleotide polymorphisms (SNPs). Although the importance of CNVs in genome wide association studies (GWAS) is becoming widely accepted, the optimal methods for identifying these variants are still under evaluation. We have previously reported a comprehensive view of CNVs in the HapMap DNA collection using high density 500K EA (Early Access) SNP genotyping arrays which revealed greater than 1,000 CNVs ranging in size from 1kb to over 3Mb. Although the arrays used most commonly for GWAS predominantly interrogate SNPs, CNV identification and detection does not necessarily require the use of DNA probes centered on polymorphic nucleotides and may even be hindered by the dependence on a successful SNP genotyping assay. Results In this study, we have designed and evaluated a high density array predicated on the use of non-polymorphic oligonucleotide probes for CNV detection. This approach effectively uncouples copy number detection from SNP genotyping and thus has the potential to significantly improve probe coverage for genome-wide CNV identification. This array, in conjunction with PCR-based, complexity-reduced DNA target, queries over 1.3M independent NspI restriction enzyme fragments in the 200bp to 1100bp size range, which is a several fold increase in marker density as compared to the 500K EA array. In addition, a novel algorithm was developed and validated to extract CNV regions and boundaries. Conclusions Using a well-characterized pair of DNA samples, close to 200 CNVs were identified, of which nearly 50% appear novel yet were independently validated using quantitative PCR. The results indicate that non-polymorphic probes provide a robust approach for CNV identification, and the increasing precision of CNV boundary delineation should allow a more complete analysis of their genomic organization. Keywords: Copy number variation (CNV) detection
2008-04-24 | GSE9053 | GEO
Project description:Avian beaks show extreme species-specific variability in morphology, though they develop from the same primordial structures. In both humans and birds, cranial neural crest cells are the primary source of mesenchyme for the frontonasal prominence; previous work has shown that these cells contain molecular information that regulate species-specific facial variation. To determine the molecular basis of avian craniofacial patterning, we have gene expression profiled micro-dissected cranial neural crest cells from the frontonasal prominence of three bird species (chickens, quails, and ducks) during embryonic development. These changes in gene expression were measured on a custom built, cross-species, long oligonucleotide microarray that interrogates the vast majority of transcription factor (TF) genes plus a wide variety of signaling pathways. Samples were isolated at two developmental stages, before (Hamilton Hamburger stage [HH] 20) and after (HH25) morphological distinctions between the species are evident. Keywords: cross-species comparison
2009-12-03 | GSE11027 | GEO
Project description:Avian beaks show extreme species-specific variability in morphology, though they develop from the same primordial structures. In both humans and birds, cranial neural crest cells are the primary source of mesenchyme for the frontonasal prominence; previous work has shown that these cells contain molecular information that regulate species-specific facial variation. To determine the molecular basis of avian craniofacial patterning, we have gene expression profiled micro-dissected cranial neural crest cells from the frontonasal prominence of three bird species (chickens, quails, and ducks) during embryonic development. These changes in gene expression were measured on a custom built, cross-species, long oligonucleotide microarray that interrogates the vast majority of transcription factor (TF) genes plus a wide variety of signaling pathways. Samples were isolated at two developmental stages, before (Hamburger Hamilton stage [HH] 20) and after (HH25) morphological distinctions between the species are evident. Keywords: developmental time point comparison
2009-12-03 | GSE11030 | GEO
Project description:Avian beaks show extreme species-specific variability in morphology, though they develop from the same primordial structures. In both humans and birds, cranial neural crest cells are the primary source of mesenchyme for the frontonasal prominence; previous work has shown that these cells contain molecular information that regulate species-specific facial variation. To determine the molecular basis of avian craniofacial patterning, we have gene expression profiled micro-dissected cranial neural crest cells from the frontonasal prominence of three bird species (chickens, quails, and ducks) during embryonic development. These changes in gene expression were measured on a custom built, cross-species, long oligonucleotide microarray that interrogates the vast majority of transcription factor (TF) genes plus a wide variety of signaling pathways. Samples were isolated at two developmental stages, before (Hamburger Hamilton stage [HH] 20) and after (HH25) morphological distinctions between the species are evident. Keywords: cross-species comparison
2009-12-03 | GSE11029 | GEO
Project description:Avian beaks show extreme species-specific variability in morphology, though they develop from the same primordial structures. In both humans and birds, cranial neural crest cells are the primary source of mesenchyme for the frontonasal prominence; previous work has shown that these cells contain molecular information that regulate species-specific facial variation. To determine the molecular basis of avian craniofacial patterning, we have gene expression profiled micro-dissected cranial neural crest cells from the frontonasal prominence of three bird species (chickens, quails, and ducks) during embryonic development. These changes in gene expression were measured on a custom built, cross-species, long oligonucleotide microarray that interrogates the vast majority of transcription factor (TF) genes plus a wide variety of signaling pathways. Samples were isolated at two developmental stages, before (Hamburger Hamilton stage [HH] 20) and after (HH25) morphological distinctions between the species are evident. Keywords: cross-species comparison
2009-12-03 | GSE11028 | GEO
Project description:Goal: To identify copy number variation in normal individuals using high density, non-polymorphic oligonucleotide probes Background DNA sequence diversity within the human genome may be more greatly affected by copy number variations (CNVs) than single nucleotide polymorphisms (SNPs). Although the importance of CNVs in genome wide association studies (GWAS) is becoming widely accepted, the optimal methods for identifying these variants are still under evaluation. We have previously reported a comprehensive view of CNVs in the HapMap DNA collection using high density 500K EA (Early Access) SNP genotyping arrays which revealed greater than 1,000 CNVs ranging in size from 1kb to over 3Mb. Although the arrays used most commonly for GWAS predominantly interrogate SNPs, CNV identification and detection does not necessarily require the use of DNA probes centered on polymorphic nucleotides and may even be hindered by the dependence on a successful SNP genotyping assay. Results In this study, we have designed and evaluated a high density array predicated on the use of non-polymorphic oligonucleotide probes for CNV detection. This approach effectively uncouples copy number detection from SNP genotyping and thus has the potential to significantly improve probe coverage for genome-wide CNV identification. This array, in conjunction with PCR-based, complexity-reduced DNA target, queries over 1.3M independent NspI restriction enzyme fragments in the 200bp to 1100bp size range, which is a several fold increase in marker density as compared to the 500K EA array. In addition, a novel algorithm was developed and validated to extract CNV regions and boundaries. Conclusions Using a well-characterized pair of DNA samples, close to 200 CNVs were identified, of which nearly 50% appear novel yet were independently validated using quantitative PCR. The results indicate that non-polymorphic probes provide a robust approach for CNV identification, and the increasing precision of CNV boundary delineation should allow a more complete analysis of their genomic organization. A set of five genomic DNA samples containing different numbers of X chromosomes (1X to 5X sample set, including NA15510 and NA10851) were hybridized to Nsp copy number (CN) arrays in triplicate to evaluate detection of copy number variation using high density, non-polymorphic oligonucleotide probes. 6 Hapmap samples were hybridized to Nsp CN arrays to evaluate Mendelian inheritance of CNVs.
2008-04-24 | E-GEOD-9053 | biostudies-arrayexpress