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Single cell multi-omics analysis reveals novel roles for DNA methylation in sensory neuron injury responses

ABSTRACT: Single cell multi-omics analysis reveals novel roles for DNA methylation in sensory neuron injury responses

PROVIDER: PRJNA513289 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8403590_1.fastq.gz	Fastqsanger.gz
	SRR8403590_2.fastq.gz	Fastqsanger.gz
	SRR8403600_1.fastq.gz	Fastqsanger.gz
	SRR8403600_2.fastq.gz	Fastqsanger.gz
	SRR8403610_1.fastq.gz	Fastqsanger.gz

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Single cell multi-omics analysis reveals novel roles for DNA methylation in sensory neuron injury responses

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Project description:Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells], with the result that very little is known regarding how the non-myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap, given that over 80% of cutaneous fibers are unmyelinated, that they transduce such important modalities as itch, pain, temperature, touch and pressure, and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non-myelinating glia roles to nerve degeneration. We utilized RNA-seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild-type larvae and in larvae that do not have peripheral glia (foxd3 mutants) using a selective, conditional approach. Overall, the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage.

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