RNA-seq analysis of the effects of single and compound deletion of Moz (Kat6a) and/or Dlx5 during mouse craniofacial development
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE134608 | GEO | 2019/07/23
REPOSITORIES: GEO
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Project description:The Dlx homeobox genes have central roles in controlling patterning and differentiation of the brain and craniofacial primordia. In the brain, loss of Dlx function results in defects in the production, migration and differentiation of GABAergic neurons, that can lead to epilepsy. In the branchial arches, loss of Dlx function leads to craniofacial malformations that include trigeminal axon pathfinding defects. To determine how these genes function, we wish to identify the transcriptional circuitry that lies downstream of these transcription factors by comparing gene expression in wild type with Dlx mutant CNS and craniofacial tissues. 1) Compare gene expression in the maxillay branch of the first branchial arch (BA) of E10.5 wild type and Dlx2 -/- mutants. 2) Compare gene expression in the maxillary branch of the first BA of E10.5 wild type and Dlx1/2 -/- mutants. 3) Compare gene expression in wild type maxillary and mandibular branchial arches. 4) Compare gene expressionin mandibular branch of Dlx5/6 -/- mutants with wild type mandibular branch. The Dlx transcription factors are essential for controlling patterning of the brain and craniofacial primordia. In the brain, they control differentiation of GABAergic neurons of the basal ganglia. In the branchial arches, they control regional patterning. I hypothesize that there will be some conserved and some divergent mechanisms that the Dlx genes use in controlling brain and craniofacial development. We have already performed array analyses on Dlx function in the developing basal ganglia (with TGEN) by comparing expressed genes in wild type and Dlx1/2 mutants. Here we will compare gene expression in the brachial arches of wild type and Dlx mutant mice. 1) Generate E10.5 mouse embryos that are either wild type, Dlx2-/-, Dlx1/2 -/- or Dlx5/6 -/-. 2) Determine genotype by PCR. 3) Dissect branchial arches from the different genotypes. 4) Separate maxillary and mandibular branch of each branchial arch. 5) Prepare total RNA from the specimens. Obtain sufficient tissue to obtain 10 ug of total RNA - based on previous experience we anticipate that this will require ~ 10 branchial arches. We will pool the tissue from different embryos of the same genotype. 6) Send total RNA to TGEN for probe preparation, hybridization and array result analysis.
2008-06-13 | E-GEOD-4774 | biostudies-arrayexpress
Project description:We present a gene expression atlas of early mouse craniofacial development. Laser capture microdissection (LCM) was used to isolate cells from the principal critical micro-regions, whose development, differentiation and signaling interactions are responsible for the construction of the mammalian face We examined the facial mesenchyme and adjacent neuroepithelium at E8.5, at E9.5 we obtain cells from the facial mesenchyme, olfactory placode/epidermal ectoderm, underlying neuroepithileium, and emerging mandibular and maxillary arches. AT E10.5 we sampled the medial and lateral prominences, olfactory pit, multiple regions of the underlying neuroepithelium the mandibular and maxillary arches, and Rathke's pouch. Mouse emrbyos were harvested at developmental stage E8.5 , E9.5, and E10.5 and cells were captured from microregions responsible for the construction of the mammalian face. RNA was extracted, labelled, and quantified using the Mouse ST-l microarray.
2014-03-18 | E-GEOD-55965 | biostudies-arrayexpress
Project description:RNA-seq analysis of the effects of single and compound deletion of Moz (Kat6a) and/or Dlx5 during mouse craniofacial development
| PRJNA555853 | ENA
Project description:Craniofacial development depends on cell-cell interactions, coordinated cellular movement and differentiation under the control of regulatory gene networks, which include the distal-less (Dlx) gene family. However, the functional significance of Dlx5 in patterning the oropharyngeal region has remained unknown. Here we show that loss of Dlx5 leads to a shortened soft palate and an absence of the levator veli palatini, palatopharyngeus, and palatoglossus muscles that are derived from the 4th pharyngeal arch (PA), but the tensor veli palatini, derived from the 1st PA, is unaffected. Dlx5-positive cranial neural crest (CNC) cells are in direct contact with myoblasts derived from the pharyngeal mesoderm, and Dlx5 disruption leads to altered proliferation and apoptosis of CNC and muscle progenitor cells. Moreover, the FGF10 pathway is downregulated in Dlx5-/- mice, and activation of FGF10 signaling rescues CNC cell proliferation and myogenic differentiation in these mutant mice. Collectively, our results indicate that Dlx5 plays critical roles in patterning of the oropharyngeal region and development of muscles derived from the 4th PA mesoderm in the soft palate, likely via interactions between CNC-derived and myogenic progenitor cells.
2017-10-15 | GSE104163 | GEO
Project description:We present a gene expression atlas of early mouse craniofacial development. Laser capture microdissection (LCM) was used to isolate cells from the principal critical micro-regions, whose development, differentiation and signaling interactions are responsible for the construction of the mammalian face. We examined the facial mesenchyme and adjacent neuroepithelium at E8.5, at E9.5, facial mesenchyme, olfactory placode/epidermal ectoderm, underlying neuroepithileium, and emerging mandibular and maxillary arches. AT E10.5 we sampled the medial and lateral prominences, olfactory pit, multiple regions of the underlying neuroepithelium the mandibular and maxillary arches, and Rathke's pouch. For these 103 samples, laser capture microdissection from serial and bioreplicated E8.5, E.9.5, and E10.5 frozen sections was used to make RNA using the ZR RNA MicroPrep kit (Zymo). Nugen RiboSpia Ovation Pico WTA System V2 was used target amplification. We used starting total RNA of at least 2 ng. For further details about this study contact steve.potter@cchmc.org (isolation and labeling) or bruce.aronow@cchmc.org (informatics)
2014-03-18 | GSE55965 | GEO
Project description:Lck-Dlx5 induces T-cell lymphoma but the mechanism is unknown. We used microarrays to detail the global programme of gene expression underlying Dlx5-induced T-cell lymphoma T-cells were isolated from Lck-Dlx5 mice, Lck-MyrAkt2 mice and Wild type littermates for RNA extraction and hybridization on Affymetrix microarrays.
2016-06-24 | E-GEOD-83685 | biostudies-arrayexpress
Project description:The Dlx homeobox genes have central roles in controlling patterning and differentiation of the brain and craniofacial primordia. In the brain, loss of Dlx function results in defects in the production, migration and differentiation of GABAergic neurons, that can lead to epilepsy. In the branchial arches, loss of Dlx function leads to craniofacial malformations that include trigeminal axon pathfinding defects. To determine how these genes function, we wish to identify the transcriptional circuitry that lies downstream of these transcription factors by comparing gene expression in wild type with Dlx mutant CNS and craniofacial tissues. 1) Compare gene expression in the maxillay branch of the first branchial arch (BA) of E10.5 wild type and Dlx2 -/- mutants. 2) Compare gene expression in the maxillary branch of the first BA of E10.5 wild type and Dlx1/2 -/- mutants. 3) Compare gene expression in wild type maxillary and mandibular branchial arches. 4) Compare gene expressionin mandibular branch of Dlx5/6 -/- mutants with wild type mandibular branch. The Dlx transcription factors are essential for controlling patterning of the brain and craniofacial primordia. In the brain, they control differentiation of GABAergic neurons of the basal ganglia. In the branchial arches, they control regional patterning. I hypothesize that there will be some conserved and some divergent mechanisms that the Dlx genes use in controlling brain and craniofacial development. We have already performed array analyses on Dlx function in the developing basal ganglia (with TGEN) by comparing expressed genes in wild type and Dlx1/2 mutants. Here we will compare gene expression in the brachial arches of wild type and Dlx mutant mice. 1) Generate E10.5 mouse embryos that are either wild type, Dlx2-/-, Dlx1/2 -/- or Dlx5/6 -/-. 2) Determine genotype by PCR. 3) Dissect branchial arches from the different genotypes. 4) Separate maxillary and mandibular branch of each branchial arch. 5) Prepare total RNA from the specimens. Obtain sufficient tissue to obtain 10 ug of total RNA - based on previous experience we anticipate that this will require ~ 10 branchial arches. We will pool the tissue from different embryos of the same genotype. 6) Send total RNA to TGEN for probe preparation, hybridization and array result analysis. Keywords: other
2006-06-06 | GSE4774 | GEO
Project description:The lysine acetyltransferase KAT6A (MOZ, MYST3) belongs to the MYST family of chromatin regulators, facilitating histone acetylation. Dysregulation of KAT6A has been implicated in developmental syndromes and the onset of acute myeloid leukemia (AML). Previous work suggests that KAT6A is recruited to its genomic targets by a combinatorial function of histone binding PHD fingers, transcription factors and chromatin binding interaction partners. Here, we demonstrated that a winged helix domain at the N-terminus of KAT6A specifically interacts with unmethylated CpG motifs. This DNA binding function leads to the association of KAT6A to unmethylated CpG islands (CGIs) genome wide. Mutation of the essential amino acids completely abrogates the enrichment of KAT6A at CGIs. Overexpression of a KAT6A WH1 mutant has a dominant negative effect on H3K9 histone acetylation, which is comparable to the effects upon overexpression of a KAT6A HAT domain mutant. Taken together, our work revealed a previously unrecognized chromatin recruitment mechanism of KAT6A, offering a new perspective on the role of KAT6A in gene regulation and human diseases
2023-01-14 | PXD034833 | Pride
Project description:Distribution of MOZ (KAT6A) in the genome and effects of MOZ on gene expression during mouse craniofacial development
| PRJNA555846 | ENA
Project description:Lck-Dlx5 induces T-cell lymphoma but the mechanism is unknown. We used microarrays to detail the global programme of gene expression underlying Dlx5-induced T-cell lymphoma
2016-06-24 | GSE83685 | GEO