Project description:Wild-type or miR-302 knockout tissue was isolated from embryos during neurulation in replicate Performed in biological triplicate except for E7.5 WT which was in duplicate and E9.5 timepoints which were in quadruplicate. Biological replicate samples represent independent embryos. Total RNA collected with Trizol. All processing conducted at the UCLA Neuroscience Genomics Core. MouseRef-8 v2.0 Expression BeadChips.
Project description:We analyzed wildtype and miR-302 knockout embryos at E7.5 and sorted neural crest using Wnt1-Cre at E8.5 and Sox9 at E9.5 to capture miRNA differences during neural crest development
Project description:We analyzed wildtype and miR-302 knockout embryos at E7.5 and sorted neural crest using Wnt1-Cre at E8.5 and Sox9 at E9.5 to capture transcriptomic differences during neural crest development
Project description:Neural crest cells are migratory progenitor cells that contribute to nearly all tissues and organs throughout the body. Their formation, migration and differentiation are regulated by a multitude of signaling pathways, that when disrupted can lead to disorders termed neurocristopathies. While work in avian and amphibian species has revealed essential factors governing the specification and induction of neural crest cells during gastrulation and neurulation in non-mammalian species, their functions do not appear to be conserved in mice, leaving major gaps in our understanding of neural crest cell formation in mammals. Here we describe Germ Cell Nuclear Factor (GCNF/Nr6a1), an orphan nuclear receptor, as a critical regulator of neural crest cell formation in mice. Gcnf null mutant mice, exhibit a major disruption of neural crest cell formation. The purpose of this experiment is to examine gene expression changes in response to Gcnf mutation in E9.0 mouse embryos.
Project description:The aim of this study was to assess whether chronic treatment with RPV can modulate the progression of chronic liver disease, especially of non-alcoholic fatty liver disease (NAFLD), through a nutritional model in wild-type mice Mice were daily treated with RPV (p.o.) and fed with normal or high fat diet during 3 months to induce fatty liver disease
Project description:The aim of the study was to investigate whether the trefoil peptide genes, in concerted action with a miRNA regulatory network, were contributing to nutritional maintrenance. Using a Tff3 knock-out mouse model, 21 specific miRNAs were noted to be significantly deregulated when compared to the wild type strain.
