Transcription profiling of mouse embryonic cells (E9.5) with homozygous knockout of Tbx1 compared to heterozygous Tbx1 knockout

ABSTRACT: 22q11 deletion syndrome (22q11DS) is mainly characterised by cardiovascular, craniofacial, thymic and parathyroid abnormalities. Haploinsufficiency of the transcription factor, TBX1 is considered to be a major underlying cause of these defects. Mice in which Tbx1 has been mutated phenocopy 22q11DS. In order to elucidate the transcriptional pathways regulated by Tbx1, the gene expression profile of Tbx1-lacZ positive cells isolated from E9.5 Df1/Tbx1lacZ embryos (Tbx1-null) were compared to cells isolated from Tbx1+/lacZ (Tbx1-heterozygous) embryos. This analysis has led to a better understanding of the pathways important in pharyngeal and heart development. Experiment design: 3 pools of cells (biological replicates) isolated from Df1/Tbx1lacZ embryos and Tbx1+/lacZ embryos were used f

ORGANISM(S): Mus musculus

SUBMITTER: Kelly Lammerts van Bueren 

PROVIDER: E-MEXP-2096 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress