Expression data from Igf-1 -/- and Igf-1+/+ mouse cochleas
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE11821 | GEO | 2008/06/19
SECONDARY ACCESSION(S): PRJNA105917
REPOSITORIES: GEO
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Project description:Different mutations in the gene encoding humans IGF-I cause intrauterine growth retardation, postnatal growth failure, microcephaly, mental retardation, bilateral sensorineural deafness and multiple dysmorphic features. Insight into the role of IGFs in inner ear cochlear ganglion neurogenesis has come from the study of genetically modified mice. Postnatal cochlear development is severely impaired in mice Igf1-/-, which develop smaller cochlea and cochlear ganglia, an immature tectorial membrane and they display a significant decrease in the number and size of auditory neurons. We used microarrays to define the genetic signatures of Igf-1 +/+ and Igf-1-/- mouse cochea and identify the differentially expressed genes. Experiment Overall Design: Cochleae from two E18.5 were isolated from both Igf-1+/+ wild type and Igf-1-/- null mice and pooled to obtain RNA. Heterozygous male and female with a genetic background C57BL/6J were mated to obtain embryos 18.5 days post coitus (E18.5). Three independent pools were used. Cochlear tissues included the otic capsule but not vestibular tissues.
2009-02-10 | E-GEOD-11821 | biostudies-arrayexpress
Project description:Different mutations in the gene encoding humans IGF-I cause intrauterine growth retardation, postnatal growth failure, microcephaly, mental retardation, bilateral sensorineural deafness and multiple dysmorphic features. Insight into the role of IGFs in inner ear cochlear ganglion neurogenesis has come from the study of genetically modified mice. Postnatal cochlear development is severely impaired in mice Igf1-/-, which develop smaller cochlea and cochlear ganglia, an immature tectorial membrane and they display a significant decrease in the number and size of auditory neurons. We used microarrays to define the genetic signatures of Igf-1 +/+ and Igf-1-/- mouse cochea and identify the differentially expressed genes. Keywords: comparison between WT and KO
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Project description:Different mutations in the gene encoding humans IGF-I cause intrauterine growth retardation, postnatal growth failure, microcephaly, mental retardation, bilateral sensorineural deafness and multiple dysmorphic features. Insight into the role of IGFs in inner ear cochlear ganglion neurogenesis has come from the study of genetically modified mice. Postnatal cochlear development is severely impaired in mice Igf1-/-, which develop smaller cochlea and cochlear ganglia, an immature tectorial membrane and they display a significant decrease in the number and size of auditory neurons. We used microarrays to define the genetic signatures of Igf-1 +/+ and Igf-1-/- mouse cochea and identify the differentially expressed genes. Experiment Overall Design: Cochleae from two E18.5 were isolated from both Igf-1+/+ wild type and Igf-1-/- null mice and pooled to obtain RNA. Heterozygous male and female with a genetic background C57BL/6J were mated to obtain embryos 18.5 days post coitus (E18.5). Three independent pools were used. Cochlear tissues included the otic capsule but not vestibular tissues.
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