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Repression of an activity-dependent autocrine insulin signal is required for sensory neuron development in C. elegans

ABSTRACT: Repression of an activity-dependent autocrine insulin signal is required for sensory neuron development in C. elegans

PROVIDER: PRJNA564979 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10098840_1.fastq.gz	Fastqsanger.gz
	SRR10098840_2.fastq.gz	Fastqsanger.gz
	SRR10098841_1.fastq.gz	Fastqsanger.gz
	SRR10098841_2.fastq.gz	Fastqsanger.gz
	SRR10098842_1.fastq.gz	Fastqsanger.gz

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Repression of an activity-dependent autocrine insulin signal is required for sensory neuron development in C. elegans

Project description:The nervous system comprises diverse and highly specialized neuron-types, each expressing a unique set of genes that defines its functional properties. What molecular mechanisms generate diverse neuron types remains a central question in neuroscience. Our study of C. elegans chemosensory BAG neurons showed that a p38 MAP kinase (MAPK), PMK-3, is required for their proper differentiation and function (Brandt, J. and Ringstad, N. 2015). How p38 MAPKs function in neurodifferentiation is poorly understood. To better understand how pmk-3 promotes the BAG cell fate, we purified wild-type and pmk-3 mutant chemosensory BAG neurons and determined their transcriptomes using RNA-Seq. Expression of a number of genes that encode neuropeptides, including insulin-like peptides (ILPs), were up-regulated in pmk-3 mutant BAG neurons. Through analysis of mutations that restore expression of a BAG-fate marker to pmk-3 mutants, we additionally found that genes required for the release of neuropeptides, including UNC-31/CAPS, suppress pmk-3 mutant gene expression defects. These two observations suggested that the differentiation defects of pmk-3 mutants are associated with dysregulated release of peptide hormones. Indeed, we find that increased synthesis and release of ILPs from BAG during development causes a significant fraction of the gene expression and functional defects of pmk-3 mutant neurons. Together our data delineate a mechanism through which p38 MAPKs promote proper sensory neuron differentiation by inhibiting an autocrine insulin signal that represses expression of a BAG neuron fate. These findings reveal an unexpected role for insulin signaling in nervous system development and suggest that insulin-like factors are at the nexus of intrinsic genetic programs and extrinsic signaling mechanisms that regulate cell fate and neuronal differentiation.

2019-09-12 | GSE137267 | GEO

Repression of an activity-dependent autocrine insulin signal is required for sensory neuron development in C. elegans.

Project description:Nervous system development is instructed by genetic programs and refined by distinct mechanisms that couple neural activity to gene expression. How these processes are integrated remains poorly understood. Here, we report that the regulated release of insulin-like peptides (ILPs) during development of the Caenorhabditis elegans nervous system accomplishes such an integration. We find that the p38 MAP kinase PMK-3, which is required for the differentiation of chemosensory BAG neurons, limits an ILP signal that represses expression of a BAG neuron fate. ILPs are released from BAGs themselves in an activity-dependent manner during development, indicating that ILPs constitute an autocrine signal that regulates the differentiation of BAG neurons. Expression of a specialized neuronal fate is, therefore, coordinately regulated by a genetic program that sets levels of ILP expression during development, and by neural activity, which regulates ILP release. Autocrine signals of this kind might have general and conserved functions as integrators of deterministic genetic programs with activity-dependent mechanisms during neurodevelopment.

| S-EPMC6899041 | biostudies-literature

Peripheral Sensory Neuron EC-tagging experiments

Project description:Peripheral Sensory Neuron EC-tagging experiments

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Runx1 Controls Auditory Sensory Neuron Diversity (CKO)

Project description:Runx1 Controls Auditory Sensory Neuron Diversity (CKO)

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Runx1 Controls Auditory Sensory Neuron Diversity (iCKO)

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Vagal Sensory Neuron-Derived FGF3 Regulates Insulin Secretion and Energy Balance

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Silencing of odorant receptor gene expression by G protein M-NM-2M-NM-3 signaling ensures the expression of one odorant receptor per olfactory sensory neuron

Project description:Olfactory sensory neurons express just one out of a possible ~1000 odorant receptor genes, reflecting an exquisite mode of gene regulation. In one model, once an odorant receptor is chosen for expression, other receptor genes are suppressed by a negative feedback mechanism, ensuring a stable functional identity of the sensory neuron for the lifetime of the cell. The signal transduction mechanism subserving odorant receptor gene silencing remains obscure, however. Here we demonstrate in the zebrafish that odorant receptor gene silencing is dependent on receptor activity. Moreover, we show that signaling through G protein M-NM-2M-NM-3 subunits is both necessary and sufficient to suppress the expression of odorant receptor genes, and likely acts through histone methylation to maintain the silenced odorant receptor genes in transcriptionally inactive heterochromatin. These results provide new insights linking receptor activity with the epigenetic mechanisms responsible for ensuring the expression of one odorant receptor per olfactory sensory neuron. Total 6 samples were analyzed-3 controls & 3 samples

2013-12-16 | E-GEOD-53334 | biostudies-arrayexpress

Profiling Kif5A RNA targets in sensory neuron axons

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Olfactory Sensory Neuron Diversity Beyond OR Genes in mice

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Silencing of odorant receptor gene expression by G protein βγ signaling ensures the expression of one odorant receptor per olfactory sensory neuron

Project description:Olfactory sensory neurons express just one out of a possible ~1000 odorant receptor genes, reflecting an exquisite mode of gene regulation. In one model, once an odorant receptor is chosen for expression, other receptor genes are suppressed by a negative feedback mechanism, ensuring a stable functional identity of the sensory neuron for the lifetime of the cell. The signal transduction mechanism subserving odorant receptor gene silencing remains obscure, however. Here we demonstrate in the zebrafish that odorant receptor gene silencing is dependent on receptor activity. Moreover, we show that signaling through G protein βγ subunits is both necessary and sufficient to suppress the expression of odorant receptor genes, and likely acts through histone methylation to maintain the silenced odorant receptor genes in transcriptionally inactive heterochromatin. These results provide new insights linking receptor activity with the epigenetic mechanisms responsible for ensuring the expression of one odorant receptor per olfactory sensory neuron.

2013-12-16 | GSE53334 | GEO

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