Effect of unilateral naris occlusion on gene profile in mouse olfactory mucosa.
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ABSTRACT: Unilateral naris occlusion was performed the day after birth in three FVB strain mice. At 25 days of age olfactory mucosa was collected from open nasal fossa, the occluded nasal fossa and from three untreated mice. Total RNA was extracted and gene profiles among these three treatment conditions were compared. The goal of the study was to determine the effect of stimulus deprivation on the genetic profile of olfactory mucosa.
Project description:Unilateral naris occlusion was performed the day after birth in three FVB strain mice. At 25 days of age olfactory mucosa was collected from open nasal fossa, the occluded nasal fossa and from three untreated mice. Total RNA was extracted and gene profiles among these three treatment conditions were compared. The goal of the study was to determine the effect of stimulus deprivation on the genetic profile of olfactory mucosa. There were three treatment conditions: open mucosa, occluded mucosa, and untreated mucosa. Each of these conditions had three biological replicates. Open and occluded however were repeated measures i.e. from the same individuals.
Project description:The objectives of this study were to use unilateral naris occlusion (UNO) to characterize the effects of olfactory deprivation on 1) gene expression changes within individual cells of the (OE) and 2) changes in the relative abundance of distinct cell types and subtypes.
Project description:The objectives of this study were to use unilateral naris occlusion (UNO) in order to characterize the effects of olfactory deprivation on the relative abundance of newly generated olfactory sensory neurons that express specific odorant receptors.
Project description:We have identified a replication-independent histone variant, Hist2h2be (referred to herein as H2be), which is expressed exclusively by olfactory chemosensory neurons. Levels of H2BE are heterogeneous among olfactory neurons, but stereotyped according to the identity of the co-expressed olfactory receptor (OR). Gain- and loss-of-function experiments demonstrate that changes in H2be expression affect olfactory function and OR representation in the adult olfactory epithelium. We show that H2BE expression is reduced by sensory activity and that it promotes neuronal cell death, such that inactive olfactory neurons display higher levels of the variant and shorter life spans. Post-translational modifications (PTMs) of H2BE differ from those of the canonical H2B, consistent with a role for H2BE in altering transcription. We propose a physiological function for H2be in modulating olfactory neuron population dynamics to adapt the OR repertoire to the environment. The objective of generating this dataset was to analyze the effects of H2be loss of function on gene expression changes in the main olfactory epithelium as a result of activity deprivation through unilateral naris occlusion (UNO). This dataset compares gene expression in wild type and H2be-KO main olfactory epithelium (MOE) samples from 5-week old mice that were subjected to unilateral naris occlusion (UNO) for 3 weeks starting from 2 weeks of age. Samples consist of MOE halves that were dissected and carefully removed from the medial bone. Each sample contains tissue from 2 mice (1 female and 1 male). There are three replicates for each genotype (H2be-KO or WT) and UNO side (open or closed) combination.
Project description:Three wild type mice with left naris occlusion were dissected for OBs. Total six OBs were used for searching the genes decreased after left naris occlusion.
Project description:We have identified a replication-independent histone variant, Hist2h2be (referred to herein as H2be), which is expressed exclusively by olfactory chemosensory neurons. Levels of H2BE are heterogeneous among olfactory neurons, but stereotyped according to the identity of the co-expressed olfactory receptor (OR). Gain- and loss-of-function experiments demonstrate that changes in H2be expression affect olfactory function and OR representation in the adult olfactory epithelium. We show that H2BE expression is reduced by sensory activity and that it promotes neuronal cell death, such that inactive olfactory neurons display higher levels of the variant and shorter life spans. Post-translational modifications (PTMs) of H2BE differ from those of the canonical H2B, consistent with a role for H2BE in altering transcription. We propose a physiological function for H2be in modulating olfactory neuron population dynamics to adapt the OR repertoire to the environment. The objective of generating this dataset was to analyze the effects of H2be loss of function on gene expression changes in the main olfactory epithelium as a result of activity deprivation through unilateral naris occlusion (UNO).
Project description:TRAP-seq of newly generated olfactory sensory neurons from the open and closed sides of the mouse olfactory epithelium following unilateral naris occlusion
Project description:Nasal mucosa and olfactory bulb are separated by the cribriform plate which is perforated by olfactory nerves. We have previously demonstrated that the cribriform plate is permissive for T cells and monocytes and that viruses can enter the bulb upon intranasal injection by axonal transportation. Therefore, we hypothesized that nasal mucosa and olfactory bulb are equipped to deal with constant infectious threats. To detect genes involved in this process, we compared gene expression in nasal mucosa and bulb of mice kept under specific pathogen free (SPF) conditions to gene expression of mice kept on non-SPF conditions using RNA deep sequencing. We found massive alterations in the expression of immune-related genes of the nasal mucosa, while the bulb did not respond immunologically. The absence of induction of immune-related genes in the olfactory bulb suggests effective defence mechanisms hindering entrance of environmental pathogens beyond the outer arachnoid layer. The genes detected in this study may include candidates conferring susceptibility to meningitis.