Project description:The trithorax H3K4 histone methyltransferase (HMT) MLL1 has important roles for early embryonic development, hematopoiesis and neurogenesis through regulation of Hox and homeodomain factor expression. MLL1 has been previously implicated in activation of Myf5 expression through an interaction with Pax7. Here, we find that in vivo, MLL1 is necessary for efficient muscle regeneration, and for maintenance of muscle stem and progenitor cells. Loss of MLL1 in cultured myoblasts reveals an essential role for proliferation and expression of both Myf5 and Pax7. Loss of Myf5 is conditional on loss of Pax7 and exogenous Pax7 rescues Myf5 in the absence of MLL1 suggesting a role for MLL1 in Pax7 expression but not Pax7 activity. Importantly, Mll1 knockout results in a minor decrease to H3K4me3 at Pax7, a 40% decrease in Pax7 mRNA and an 85% decrease in Pax7 protein, suggesting a previously proposed non-HMT role for MLL1 may involve linking transcription to translation.
Project description:This study aims at giving an insight on gene expression in CCAM. Keywords: disease state analysis A total of 14 microarrays were completed. Samples were divided into four groups: Fetal CCAM samples (n=4), fetal control samples (n=2), post-natal CCAM samples (n=5), post-natal control samples (n=3)
Project description:Although there have been studies conducted on cornea and retina growth and development, postnatal gene expression studies on sclera growth during postnatal growth has not been well characterised. Given that the mouse genome has 85% homology to the human genome and has been completely sequenced, mouse model for the study of ocular growth has advantages over other animal models. Thus, we aimed to study the biology and genetics behind sclera growth during post-natal development in Balb/cJ mice as a means to understand genetic changes that cause scleral growth and development during post-natal eye development The purpose of this study was to identify the genes underlying the development of mouse sclera post-natal growth of the posterior chamber of the eye using microarray
Project description:We have compared the gene expression profile of post-natal 1 day and 7 day rat Achilles tendons. Post-natal 1 day and 7 day rat Achilles tendons were collected. Each sample contains at least two individuals. Total RNA was extracted and fragmented biotin-tagged cRNA was hybridized to Rat Genome 230 2.0 Array.
Project description:During the studies of post-natal lung development in the laboratory C57BL/6 mouse, broad spectrums of interventions are applied by intraperitoneal (i.p.) injections. We explored whether injection of saline, tamoxifen, “scrambled” antagomiRs (to control studies that target microRNA with antagomiRs), migloyl or water, in well-established protocols, had any impact on the post‑natal gene expression in mouse lungs.
Project description:The liver is a multifunctional organ, which undergoes rapid changes during the developmental period and relies on tightly-regulated gene expression. Little is known regarding the complex expression patterns of mRNAs during the early stages of human liver development in comparison to post-natal livers. We used microarrays to detail the global programme of gene expression during liver development following specification, at the stage of proliferation and differentiation when compared to post-natal livers, and identified distinct classes of up-regulated and downregulated genes during this process.
Project description:Due to the vital importance of the Central Nervous System (CNS), its potential infection and inflammation have to be tightly controlled. The surface of the CNS is connected to the periphery by a rich and complex tissue, the meninges. They contain a vast network of macrophages subdivided in at least two subpopulations endowed with elusive functions: a neonatal, MHC-II negative macrophage population, and an post-natal population expressing MHC-II. Using in situ-histocytometry, flow cytometry, and single-cell RNA sequencing approaches, we showed that those populations have opposite dynamic behaviors in response to in vivo peripheral challenges such as LPS, SARS-CoV2 and lymphocytic choriomeningitis virus (LCMV), with an apparent contraction of the MHC-II+ population. Focusing on LCMV infection in experimental mouse models and using innovative pharmacological and genetic depletion strategies, we show that meningeal macrophages (MM) represent an early line of protection against this neuroinvasive pathogen. In their absence, specific areas in the meninges became highly infected, leading to fatal brain disease. While their intrinsic sensing of viral replication through the Mitochondrial antiviral-signaling protein (MAVS) was dispensable, sensing of IFNs through the STAT1 pathway played an important role in controlling viral spread. Unexpectedly, the post-natal MHC-II+ macrophage population had an important role in controlling neuroinfection, by shutting down biosynthesis pathways and efficiently blocking viral replication. This work helps understanding the spatial organization of the brain defense system and the cellular and molecular mechanisms involved in CNS protection.