Expression data from mesodermal Tbx1-knockout ears, otic vesicles, and periotic mesenchyme
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Tingwei Guo
PROVIDER: E-GEOD-34066 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The T-box transcription factor Tbx1 is expressed in the otic vesicle and surrounding periotic mesenchyme during inner ear development. Mesenchymal Tbx1 is essential for inner ear development, with conditional mutants displaying defects in both auditory and vestibular systems. We have previously identified reduced expression of retinoic acid metabolic genes in the periotic mesenchyme of mesoderm conditional Tbx1 mutants, using the T-Cre mouse line, implicating retinoic acid in mesenchymal-epithelial signaling downstream of Tbx1 in the periotic mesenchyme. In order to identify downstream effectors of mesenchymal-epithelial signaling downstream of mesenchymal Tbx1, we have utilized a gene profiling approach comparing embryonic day 11.5 otic vesicle and surrounding periotic mesenchyme from T-Cre-mediated conditional Tbx1 mutants (Mest-KO) and conditional heterozygous control litter mates (control). This data was used in conjunction with OV-only data (GSE34064) to identify expression changes within the periotic mesenchyme. E11.5 T-Cre-mediated conditional Tbx1 mutants (Mest-KO) and control (T-Cre conditional Tbx1 heterozygotes) embryos were microdissected to isolate the otic vesicle and surrounding periotic mesenchyme. Left and right ears from 3 embryos of the same genotype were pooled for each chip, and 3 biological replicates of each chip were performed.
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Project description:The T-box transcription factor Tbx1 is expressed in the otic vesicle and surrounding periotic mesenchyme during inner ear development. Mesenchymal Tbx1 is essential for inner ear development, with conditional mutants displaying defects in both auditory and vestibular systems. We have previously identified reduced expression of retinoic acid metabolic genes in the periotic mesenchyme of mesoderm conditional Tbx1 mutants, using the T-Cre mouse line, implicating retinoic acid in mesenchymal-epithelial signaling downstream of Tbx1 in the periotic mesenchyme. In order to identify downstream effectors of mesenchymal-epithelial signaling downstream of mesenchymal Tbx1, we have utilized a gene profiling approach comparing embryonic day 11.5 otic vesicle tissue from T-Cre-mediated conditional Tbx1 mutants (Mest-KO) and conditional heterozygous control litter mates (control). E11.5 T-Cre-mediated conditional Tbx1 mutants (Mest-KO) and control (T-Cre conditional Tbx1 heterozygotes) embryos were microdissected to isolate the otic vesicle. Left and right ears from 3 embryos of the same genotype were pooled for each chip.
2013-01-01 | E-GEOD-34064 | biostudies-arrayexpress
Project description:The T-box transcription factor Tbx1 is expressed in the otic vesicle and surrounding periotic mesenchyme during inner ear development. Mesenchymal Tbx1 is essential for inner ear development, with conditional mutants displaying defects in both auditory and vestibular systems. We have previously identified reduced expression of retinoic acid metabolic genes in the periotic mesenchyme of mesoderm conditional Tbx1 mutants, using the T-Cre mouse line, implicating retinoic acid in mesenchymal-epithelial signaling downstream of Tbx1 in the periotic mesenchyme. In order to identify downstream effectors of mesenchymal-epithelial signaling downstream of mesenchymal Tbx1, we have utilized a gene profiling approach comparing embryonic day 12.5 periotic tissue from T-Cre-mediated conditional Tbx1 mutants (Mest-KO) and conditional heterozygous control litter mates (control). E12.5 T-Cre-mediated conditional Tbx1 mutants (Mest-KO) and control (T-Cre conditional Tbx1 heterozygotes) embryos were microdissected to isolate the otic vesicle and surrounding periotic mesenchyme. Left and right tissue from each individual embryo was pooled, and 5 control and 5 mutant embryos were analyzed on individual microarrays using Affymetrix Mouse Gene ST 1.0 chips.
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Project description:The infant leukemia-associated gene, Ott1(Rbm15), has broad regulatory effects within the murine hematopoiesis. However, germline Ott1 deletion results in fetal demise prior to E10.5, indicating additional developmental requirements for Ott1. The spen gene family, to which Ott1 belongs, has a transcriptional activation/repression domain and RNA recognition motifs, and in Drosophila has a significant role in the development of the head and thorax. Early Ott1-deficient embryos show growth retardation and incomplete closure of the notochord. Further analysis demonstrated placental defects in the spongiotrophoblast and syncytiotrophoblast layers, resulting in an arrest of vascular branching morphogenesis. Rescue of the placental defect using a conditional allele with a trophoblast-sparing cre transgene allowed embryos to form a normal placenta and survive gestation. This result shows that the process of vascular branching morphogenesis in Ott1-deficient animals is regulated by the trophoblast compartment rather than the fetal vasculature. Mice surviving to term manifested hyposplenia and abnormal cardiac development. Analysis of global gene expression of Ott1-deficient embryonic hearts shows enrichment of hypoxia-related genes and significant alteration of several candidate genes critical for cardiac development. Thus, Ott1-dependent pathways in addition to being implicated in leukemogenesis, may also be important in the pathogenesis of placental insufficiency and cardiac malformations. Experiment Overall Design: We generated in triplicate mice containing the Ott1flox and Ott1null alleles. Tg-Sox2-cre animals were obtained from Jackson labs (Bar Harbor, ME). Genotyping was performed by PCR analysis of murine or embryonic tissue [Raffel, 2007 #218]. Timed matings were determined by presence of a vaginal plug at E0.5. Experiment Overall Design: RNA was extracted from 3 hearts each from either Ott1null/nullSox2-cre or Ott1null/wtSox2-cre E18.5 embryos using the RNeasy Micro kit (Qiagen, Valencia, CA) and treated with RNAse-free DNAse (Qiagen, Valencia, CA). 50 ng of purified total RNA was linearly amplified using the Ovation RNA amplification system V2 (Nugen, San Carlos, CA) and biotinylated with the FL-Ovation Biotin Module V2 (Nugen, San Carlos, CA) per the supplied protocol. cDNA was then hybridized to Affymetrix Mouse expression array 430A2.0 chips by the Dana Farber Microarray Core Facility (Boston, MA). The raw gene expression values were preprocessed with robust multi-array analysis (RMA) algorithm using BioConductor software.
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