Glial cells maintain synapses by inhibiting an activity-dependent retrograde protease signal
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA516573 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8476250.fastq.gz | Fastqsanger.gz | |||
| SRR8476251.fastq.gz | Fastqsanger.gz | |||
| SRR8476252.fastq.gz | Fastqsanger.gz | |||
| SRR8476247.fastq.gz | Fastqsanger.gz | |||
| SRR8476248.fastq.gz | Fastqsanger.gz |
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Project description:Glial cells regulate multiple aspects of synaptogenesis. In the absence of Schwann cells, a peripheral glial cell, motor neurons initially innervate muscle but then degenerate. Here, using a genetic approach, we show that neural activity-regulated negative factors produced by muscle drive neurodegeneration in Schwann cell-deficient mice. We find that thrombin, the hepatic serine protease central to the hemostatic coagulation cascade, is one such negative factor. Trancriptomic analysis shows that expression of the antithrombins serpin C1 and D1 is significantly reduced in Schwann cell-deficient mice. In the absence of peripheral neuromuscular activity, neurodegeneration is completely blocked, and expression of prothrombin in muscle is markedly reduced. In the absence of muscle-derived prothrombin, neurodegeneration is also markedly reduced. Together, these results suggest that Schwann cells regulate NMJs by opposing the effects of activity-regulated, muscle-derived negative factors and provide the first genetic evidence that thrombin plays a central role outside of the coagulation system.
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Project description:To analyze the impact of photosynthetic redox signals, light sources with spectral qualities that preferentially excite either Photosystem I (PSI light) or Photosystem II (PSII light) were used. The light sources have been described in (Wagner et al, Planta 2008). Strong reduction signals were induced by light shifts from PSI to PSII light (PSI-II). In order to find primary regulated genes the acclimation responses were monitored at 30 min and 60 min after a light shift. The control was continuous Psi light at the same time. We used stn7 (a thylakoid redox regulated kinase) to specifically block transduction of photosynthetic redox signal in order to compare “real” redox regulated with that of other light acclimation pathways. Keywords: photosynthesis, redox regulation, light acclimation, retrograde signalling, long term response
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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:Motor axons receive retrograde signals from skeletal muscle that are essential for the differentiation and stabilization of motor nerve terminals. Identification of these retrograde signals has proved elusive, but their production by muscle depends on the receptor tyrosine kinase, MuSK (muscle, skeletal receptor tyrosine-protein kinase), and Lrp4 (low-density lipoprotein receptor (LDLR)-related protein 4), an LDLR family member that forms a complex with MuSK, binds neural agrin and stimulates MuSK kinase activity. Here we show that Lrp4 also functions as a direct muscle-derived retrograde signal for early steps in presynaptic differentiation. We demonstrate that Lrp4 is necessary, independent of MuSK activation, for presynaptic differentiation in vivo, and we show that Lrp4 binds to motor axons and induces clustering of synaptic-vesicle and active-zone proteins. Thus, Lrp4 acts bidirectionally and coordinates synapse formation by binding agrin, activating MuSK and stimulating postsynaptic differentiation, and functioning in turn as a muscle-derived retrograde signal that is necessary and sufficient for presynaptic differentiation.
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Project description:The transcriptional events accompanying synaptogenesis are largely unknown, or have been studied in systems in which synapse formation occurs gradually over time. With a system in which synaptogenesis is synchronized and controllable, molecular or biochemical techniques can be used to examine cellular events across cultures on a wide scale, as synapses develop. Here, we have triggered synaptogenesis in immunopurified subplate neurons by coculturing with cortical feeder layers and have used microarrays to investigate the transcriptional events occuring in this more defined and controllable system. Experiment Overall Design: Affymetrix rat GeneChip microarrays were used to assess whether coculturing induces transcriptional changes in subplate neurons. Subplate synapses develop rapidly following coculturing; an exposure to the feeder layer of only 48 hours is sufficient to detect a significant increase in the density of synapses, and is as effective as longer durations. Within the first few minutes or hours of a cell's response to an exogenous signal, any primary transcriptional events are expected to involve activation of immediate early genes (IEGs), often transcription factors themselves, which may then turn on downstream target response genes encoding factors to be delivered to sites of action, such as synapses. With the aim of searching for such downstream genes, microarrays were performed after 24 hours of coculturing, an intermediate timepoint between the likely phase of IEG transcription and the large wave of synaptogenesis seen between 24 and 48 hours of coculturing. Additional microarrays were also performed after 96 hours of coculturing to assess transcriptional changes that might occur over longer timescales. Five biological replicates of control and cocultured neurons at 24 and 96 hours were used, for a total of 20 microarrays.
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