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Deconvoluting ACS1 retrograde signaling networks that regulate leaf development

ABSTRACT: Deconvoluting ACS1 retrograde signaling networks that regulate leaf development

PROVIDER: PRJNA638809 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12017002.fastq.gz	Fastqsanger.gz
	SRR12017003.fastq.gz	Fastqsanger.gz
	SRR12017004.fastq.gz	Fastqsanger.gz
	SRR12017005.fastq.gz	Fastqsanger.gz
	SRR12017006.fastq.gz	Fastqsanger.gz

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Deconvoluting ACS1 retrograde signaling networks that regulate leaf development

Project description:Signals originating within plastids modulate organelle differentiation by transcriptionally regulating nuclear-encoded genes. These retrograde signals are also integral regulators of plant development, including leaf morphology. The clb5 mutant displays severe leaf morphology defects due to Apocarotenoid Signal 1 (ACS1) accumulation in the developmentally arrested plastid. Transcriptomic analysis of clb5 validates ACS1 as a true retrograde signal impacting expression of hundreds of nuclear genes, including suppression of most genes encoding plastid ribosomal proteins.

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Project description:Retrograde signaling from axon to soma activates intrinsic regeneration mechanisms in lesioned peripheral sensory neurons; however, the links between axonal injury signaling and the cell body response are not well understood. Here, we used phosphoproteomics and microarrays to implicate ~900 phosphoproteins in retrograde injury signaling in rat sciatic nerve axons in vivo and ~4500 transcripts in the in vivo response to injury in the dorsal root ganglia. Computational analyses of these data sets identified ~400 redundant axonal signaling networks connected to 39 transcription factors implicated in the sensory neuron response to axonal injury. Experimental perturbation of individual overrepresented signaling hub proteins, including Abl, AKT, p38, and protein kinase C, affected neurite outgrowth in sensory neurons. Paradoxically, however, combined perturbation of Abl together with other hub proteins had a reduced effect relative to perturbation of individual proteins. Our data indicate that nerve injury responses are controlled by multiple regulatory components, and suggest that network redundancies provide robustness to the injury response Microarrays were run on mRNA extracted from adult rat L4 and L5 DRGs cells after 1,3,8,12,16,18,24, and 28 hours after a sciatic nerve (proximal and distal) lesion.

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