Local translation highlights novel properties of perisynaptic astrocytic processes, and is modulated by behavior involving the dorsal hippocampus
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ABSTRACT:
PROVIDER: PRJNA600885 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10877100.fastq.gz | Fastqsanger.gz | |||
| SRR10877101.fastq.gz | Fastqsanger.gz | |||
| SRR10877102.fastq.gz | Fastqsanger.gz | |||
| SRR10877103.fastq.gz | Fastqsanger.gz | |||
| SRR10877104.fastq.gz | Fastqsanger.gz |
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Project description:Local translation is a conserved molecular mechanism. It allows a cell with a complex shape to bypass somatic protein synthesis and transport, and thus to respond quickly to a local stimulus. Local translation also contributes to the establishment of molecular and functional polarity. In the brain, it has been extensively studied in neurons and has also been described more recently in astrocytes - a type of glial cell with specialized extensions that contact vessels and synapses. Here, we studied perisynaptic astrocytic processes (PAPs) in the dorsal hippocampus and showed that they contain RNAs, ribosomes, the endoplasmic reticulum-Golgi intermediate compartment, particles of the Golgi apparatus, and protein synthesis events. We used our recently refined polysome immunoprecipitation technique to characterize the pool of polysomal mRNAs in PAPs (which we refer to as the “PAPome”) from the dorsal hippocampus and compared it with the polysomal mRNAs found in the astrocyte as a whole. The polysomal transcripts that were enriched in the PAPome encoded mostly cytoplasmic proteins and defined an unexpected molecular repertoire with the most enriched transcripts coding for proteins involved in iron homeostasis, translation, cell cycle and cytoskeleton. Interestingly, among them Erz, Fth1, and Rplp1 were enriched in PAPs compared to perivascular astrocytic processes indicating that local translation differ at these two interfaces and may sustain distinct molecular properties. The PAP-enriched transcripts Flt1, Fth1, Ccnd2, Mdm2, Gnb2l1 and Eef1a1 code for proteins involved in memory and learning mechanisms. We therefore studied their local translation in the context of fear conditioning (i.e. behavior involving the dorsal hippocampus). We observed changes in the density and/or distribution of these mRNAs in astrocytes processes as well as a drop of their translation specifically in PAPs. Our results highlight unexpected molecular properties of hippocampal PAPs and suggest for the first time that local translation in this perisynaptic compartment is linked to fear-related memory.
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Project description:This study aims at investigating differential gene expression in human astrocytic tumours of grades I, II, III and IV. A total of 65 tumours were assessed using the Affymetrix U133A GeneChip. The study aims not only at discovering the main expression differences between astrocytic tumours of distinct histological grades but also wishes to correlate these findings with the known histopathological hallmarks of astrocytoma progression. Further, the study aims at correlating gene expression with previously obtained genomic information for several loci known to be involved in astrocytoma tumour progression.
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Project description:Astrocyte activation is a common feature of neurodegenerative diseases. However, the ways in which dying neurons influence the activity of astrocytes is poorly understood. RIPK3 signaling has recently been described as a key regulator of neuroinflammation, but whether this kinase mediates astrocytic responsiveness to neuronal death has not yet been studied. Here, we used the MPTP model of Parkinson’s disease to show that activation of astrocytic RIPK3 drives dopaminergic cell death and axon damage. Transcriptomic profiling revealed that astrocytic RIPK3 promoted gene expression associated with neuroinflammation and movement disorders, and this coincided with significant engagement of DAMP signaling. Using human cell culture systems, we show that factors released from dying neurons signal through RAGE to induce RIPK3-dependent astrocyte activation. These findings highlight a mechanism of neuron-glia crosstalk in which neuronal death perpetuates further neurodegeneration by engaging inflammatory astrocyte activation via RIPK3.
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Project description:The morphology of astrocytic processes determines their close structural association with synapses referred to as the 'tripartite synapse'. Concerted morphological plasticity processes at tripartite synapses are supposed to shape neuronal communication. Morphological changes in astrocytes as well as the motility of astrocytic processes require remodeling of the actin cytoskeleton. Among the regulators of fast timescale actin-based motility, the actin binding protein profilin 1 has recently been shown to control the activity-dependent outgrowth of astrocytic processes. Here, we demonstrate that cultured murine astrocytes in addition to the ubiquitous profilin 1 also express the neuronal isoform profilin 2a. To analyze the cellular function of both profilins in astrocytes, we took advantage of a shRNA mediated isoform-specific downregulation. Interestingly, consistent with earlier results in neurons, we found redundant as well as isoform-specific functions of both profilins in modulating cellular physiology. The knockdown of either profilin 1 or profilin 2a led to a significant decrease in cell spreading of astrocytes. In contrast, solely the knockdown of profilin 2a resulted in a significantly reduced morphological complexity of astrocytes in both dissociated and slice culture astrocytes. Moreover, both isoforms proved to be crucial for forskolin-induced astrocytic stellation. Furthermore, forskolin treatment resulted in isoform-specific changes in the phosphorylation level of profilin 1 and profilin 2a, leading to a PKA-dependent phosphorylation of profilin 2a. In addition, transwell assays revealed an involvement of both isoforms in the motility of astrocytic processes, while FRAP analysis displayed an isoform-specific role of profilin 1 in the regulation of actin dynamics in peripheral astrocytic processes. Taken together, we suggest profilin isoforms to be important modulators of astrocytic morphology and motility with overlapping as well as isoform-specific functions.
| S-EPMC4309604 | biostudies-literature