Project description:To study the development of pig facial skin after birth, we use the facial skin tissues of healthy Chenghua sows as experimental materials. we then performed gene expression profiling analysis using data obtained from RNA-seq of pig facial skin tissues at four time points.
Project description:Expression of known and predicted genes in tissues of Xenopus tropicalis (frog) pooled from multiple healthy individuals. Two-colour experiments with two different tissues hybridized to each array. Each tissue is arrayed in replicate with dye swaps. Tissues: Brain, Cartilage, Esophagus, Eye, Fat body, Femur, Gallbladder, Heart, Kidney, Large intestine, Liver, Lung, Muscle, Ovary, Oviduct, Skin, Small intestine, Spleen, Stomach, Testis
Project description:Setleis Syndrome is a rare type of facial ectodermal dysplasia characterized by an aged leonine appearance with puckered skin about the eyes, absent eyelashes on both lids or multiple rows on the upper lids and none on the lower lids, eyebrows that slant sharply upward laterally, and a rubbery feel of the nose and chin. Some of the patients showed bilateral temporal marks superficially like forceps marks and like the lesions seen in focal facial dermal dysplasia. We have evidence that Setleis Syndrome is caused by nonsense mutations in the gene coding for the small bHLH transcription factor known as TWIST2 in Puerto Rican and Omani patients. We performed expression microarray analysis of RNA samples derived from skin fibroblasts grown from skin biopsies of Setleis Syndrome patients and normal controls in order to identify genes potentially involved in facial development and the pathogenesis of Setleis Syndrome. A total of 4 control and 4 Setleis Syndrome RNA samples were hybridized to U133 plus 2 Affymetrix 3'IVT arrays in the Mount Sinai School of Medicine Microarray Core Facility.
Project description:A 640kb non-coding interval at 8q24 has been associated with an increased risk of non-syndromic cleft lip and palate (CLP) in humans, but the genes and pathways involved in this genetic susceptibility have remained elusive. With a large series of rearrangements engineered over the syntenic mouse region, we showed that this interval contains very remote cis-acting enhancers that control c-myc expression in the developing face. Deletion of this interval led to mild alteration of facial morphologies in mice and, sporadically, to CLP. At a molecular level, we identified mis-expression of several downstream genes, highlighting a combined impact on cranio-facial developmental network and general metabolic capacity. This dual molecular etiology may account for the prominent role to the 8q24 region in human facial dysmorphologies. ChIP-seq and transcriptomics analysis in wt or/and mutant mice
