Effects of Bcl11b-deficiency on gene expression in the main olfactory epithelium of neonatal mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE90798 | GEO | 2018/12/31
REPOSITORIES: GEO
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Project description:Individual olfactory sensory neurons (OSNs) express a single odorant receptor (OR) gene from the class I or class II repertoire in mice. The mechanisms that regulate the binary fate specification of OSNs remain unknown. Here we show that the transcription factor Bcl11b, which is expressed in class II OSNs determines the OR class to be expressed in OSNs. Genetic studies provide evidence that class I is a default-fate and Bcl11b permits a class II fate by suppressing a class I-OR enhancer. These findings reveal a unique transcriptional mechanism that serves as a binary switch to select the OR class and is crucial to both the anatomical and functional organization of olfactory system.
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Project description:The goal of this study was to identify those odorant receptors conferring a response to indole or related odorants (2-methylindole, 3-methylindole, 6-methylindole, 2-methoxynaphthalene, and Lilyflore®) in olfactory sensory neurons (OSNs). Odorants were sequentially delivered to dissociated OSNs, and six OSNs with three different response profiles were isolated for transcriptome analysis. OSN1 and OSN2 responded to indole, 2-methylindole, 3-methylindole, and 6-methylindole; OSN3 and OSN4 responded to Indole and 2-methoxynaphthalene; OSN5 and OSN6 responded to indole, 3-methylindole, 6-methylindole, and 2-methoxynaphthalene. RNA transcripts encoding Olfr740 (OSN1, OSN2), Olfr741 (OSN3, OSN4), and Olfr743 (OSN5, OSN6) were retrieved, with high level expression of a single OR transcript in each OSN. The expression of mature OSN markers OMP, Golf, Adcy3, Cnga2 and Rtp1 was also confirmed.
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Project description:Olfactory sensory neurons (OSNs) are functionally defined by their expression of a unique odorant receptor (OR). Mechanisms underlying singular OR expression are well studied, and involve a massive cross-chromosomal enhancer interaction network. Trace amine-associated receptors (TAARs) form a distinct family of olfactory receptors, and here we find that mechanisms regulating Taar gene choice display many unique features. The epigenetic signature of Taar genes in TAAR OSNs is different from that in OR OSNs. We further identify that two TAAR enhancers conserved across placental mammals are absolutely required for expression of the entire Taar gene repertoire. Deletion of either enhancer dramatically decreases the expression probabilities of different Taar genes, while deletion of both enhancers completely eliminates the TAAR OSN populations. In addition, both of the enhancers are sufficient to drive transgene expression in the partially overlapped TAAR OSNs. We also show that the TAAR enhancers operate in cis to regulate Taar gene expression. Our findings reveal a coordinated control of Taar gene choice in OSNs by two remote enhancers, and provide an excellent model to study molecular mechanisms underlying formation of an olfactory subsystem.
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Project description:Olfactory sensory neurons (OSNs) are functionally defined by their expression of a unique odorant receptor (OR). Mechanisms underlying singular OR expression are well studied, and involve a massive cross-chromosomal enhancer interaction network. Trace amine-associated receptors (TAARs) form a distinct family of olfactory receptors, and here we find that mechanisms regulating Taar gene choice display many unique features. The epigenetic signature of Taar genes in TAAR OSNs is different from that in OR OSNs. We further identify that two TAAR enhancers conserved across placental mammals are absolutely required for expression of the entire Taar gene repertoire. Deletion of either enhancer dramatically decreases the expression probabilities of different Taar genes, while deletion of both enhancers completely eliminates the TAAR OSN populations. In addition, both of the enhancers are sufficient to drive transgene expression in the partially overlapped TAAR OSNs. We also show that the TAAR enhancers operate in cis to regulate Taar gene expression. Our findings reveal a coordinated control of Taar gene choice in OSNs by two remote enhancers, and provide an excellent model to study molecular mechanisms underlying formation of an olfactory subsystem.
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Project description:Olfactory sensory neurons (OSNs) are functionally defined by their expression of a unique odorant receptor (OR). Mechanisms underlying singular OR expression are well studied, and involve a massive cross-chromosomal enhancer interaction network. Trace amine-associated receptors (TAARs) form a distinct family of olfactory receptors, and here we find that mechanisms regulating Taar gene choice display many unique features. The epigenetic signature of Taar genes in TAAR OSNs is different from that in OR OSNs. We further identify that two TAAR enhancers conserved across placental mammals are absolutely required for expression of the entire Taar gene repertoire. Deletion of either enhancer dramatically decreases the expression probabilities of different Taar genes, while deletion of both enhancers completely eliminates the TAAR OSN populations. In addition, both of the enhancers are sufficient to drive transgene expression in the partially overlapped TAAR OSNs. We also show that the TAAR enhancers operate in cis to regulate Taar gene expression. Our findings reveal a coordinated control of Taar gene choice in OSNs by two remote enhancers, and provide an excellent model to study molecular mechanisms underlying formation of an olfactory subsystem.
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Project description:Olfactory sensory neurons (OSNs) are functionally defined by their expression of a unique odorant receptor (OR). Mechanisms underlying singular OR expression are well studied, and involve a massive cross-chromosomal enhancer interaction network. Trace amine-associated receptors (TAARs) form a distinct family of olfactory receptors, and here we find that mechanisms regulating Taar gene choice display many unique features. The epigenetic signature of Taar genes in TAAR OSNs is different from that in OR OSNs. We further identify that two TAAR enhancers conserved across placental mammals are absolutely required for expression of the entire Taar gene repertoire. Deletion of either enhancer dramatically decreases the expression probabilities of different Taar genes, while deletion of both enhancers completely eliminates the TAAR OSN populations. In addition, both of the enhancers are sufficient to drive transgene expression in the partially overlapped TAAR OSNs. We also show that the TAAR enhancers operate in cis to regulate Taar gene expression. Our findings reveal a coordinated control of Taar gene choice in OSNs by two remote enhancers, and provide an excellent model to study molecular mechanisms underlying formation of an olfactory subsystem.
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