Project description:We used laser capture microdissection to isolate maxillary arch mesenchyme from E10.5 embryos. This tissue was collected from both control (3x) and Lhx6-/-;Lhx8-/- mutant (3x) samples. Transcriptional profiling was performed using Affymetrix GeneChip Mouse Genome 430 2.0 arrays.
Project description:We used laser capture microdissection to isolate maxillary arch mesenchyme from E10.5 embryos. This tissue was collected from both control (3x) and Lhx6-/-;Lhx8-/- mutant (3x) samples. Transcriptional profiling was performed using Affymetrix GeneChip Mouse Genome 430 2.0 arrays. The mutant mice are of mixed genetic background of C57BL/6J, 129 and CD-1 strains. The head of E10.5 embryos was collected and embedded in Optimal Cutting Temperature resin (Tissue-Tek) by flash freezing on dry ice. The frozen sections were collected on polyethylene naphthalate membrane slides (Leica). Leica LMD6000 Laser Micro-Dissection System was used to cut out the normal expression domain of Lhx6 and Lhx8 in the maxillary arch mesenchyme. The tissue was collected from the entire antero-posterior extent of the maxillary arches. Total RNA was extracted using RNeasy Micro Kit (Qiagen). Subsequent steps of transcriptional profiling were performed by the New York University Genome Technology Center, beginning with the amplification of RNA by Ovation Nano Amplification system (NuGen). RNA samples from three wild-type and three Lhx6−/−;Lhx8−/− mutant embryos, all somite count- and sex-matched (females), were analyzed with Affymetrix GeneChip Mouse Genome 430 2.0 arrays. A list of Lhx-regulated genes were generated from the microarray result based on the following criteria: fold change in the average expression between wild types and Lhx6−/−;Lhx8−/− mutants is >1.5, the difference is statistically significant (P < 0.05) and the average intensity of the probe signal is >100 for wild-type and/or mutant samples. The resulting list of 212 genes was used for a gene ontology analysis with DAVID (27,28).
Project description:Aim: Identify molecular pathways controlling palate closure Methods: First pharygneal arch of wild-type and Grhl2-/- e10.5 moues embryos was subjected to RNAseq Results: Grhl2-/- PA1 displayed a shift from epithelial to mesenchymal gene expression Conclusions: Grhl2 maintains epithelial cellular identity during palate closure
Project description:We performed scRNA-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO). We dissected primarily the cardiac region but also the regions dorsal to the heart and the pharyngeal arches to capture the progenitor cells that migrate into the heart and the neural crest cells. For time points E10.5 and E11.5, we primarily dissected the regions behind the heart and included less of the overall cardiac region. We included pharyngeal arches for all time points and, at E11.5, we excluded the first arch. For Tbx1 null embryos, we also generated scRNA-seq data for WT and mutant embryos from the same pool of dissociated cells used for scATAC-seq.
Project description:We performed scATAC-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO). We dissected primarily the cardiac region but also the regions dorsal to the heart and the pharyngeal arches to capture the progenitor cells that migrate into the heart and the neural crest cells. For time points E10.5 and E11.5, we primarily dissected the regions behind the heart and included less of the overall cardiac region. We included pharyngeal arches for all time points and, at E11.5, we excluded the first arch. For Tbx1 null embryos, we also generated scRNA-seq data for WT and mutant embryos from the same pool of dissociated cells used for scATAC-seq.
Project description:In the study we compared migrating embryonic cortical interneurons from control mouse embryos and ones carryng homozygous deletions of either Mtg8 or Lhx6. The aim was to identify genes that are co-regulated by LHX6 and MTG8.
