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Activity-dependent ribosome profiling reveals the landscape of canonical and non-canonical translation in brain tissue

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE317977 | GEO | 2026/03/01

REPOSITORIES: GEO

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Activity-dependent ribosome profiling reveals the landscape of canonical and non-canonical translation in brain tissue [RIP-Seq]

Project description:Neural activity-dependent translation is essential for synaptic plasticity and diverse brain functions. Translation involves not only canonical main open reading frames (mORFs) but also upstream ORFs (uORFs), which may regulate mORF expression. However, due to technical limitations, systematic in-vestigation of activity-dependent uORFs and mORFs in brain tissues remains challenging. Here, we developed a ribosome tagging and purification strategy that bypasses the prolonged turnover of ribo-somal proteins, enabling ribosome profiling with one-hour temporal resolution after neural stimulation. Applying this strategy to mouse hippocampal slices undergoing long-term potentiation, we identified hundreds of activity-induced mORFs and uORFs, a subset of which served as robust markers for ac-tivity status. Notably, ~22% of the upregulated uORFs overlapped with those induced by the integrated stress response, suggesting potential crosstalk between these signaling pathways. This study provides a useful technique and resources for deciphering molecular mechanisms underlying activity- and trans-lation-dependent brain functions in health and disease.

2026-03-01 | GSE317975 | GEO

Activity-dependent ribosome profiling reveals the landscape of canonical and non-canonical translation in brain tissue [Ribo-Seq]

2026-03-01 | GSE317973 | GEO

Activity-dependent ribosome profiling reveals the landscape of canonical and non-canonical translation in brain tissue [Ribo and RNA-Seq]

Project description:Identification hundreds of activity-induced mORFs and uORFs, a subset of which served as robust markers for activity status

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Activity-dependent ribosome profiling reveals the landscape of canonical and non-canonical translation in brain tissue

Project description:Activity-dependent ribosome profiling reveals the landscape of canonical and non-canonical translation in brain tissue

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Activity-dependent ribosome profiling reveals the landscape of canonical and non-canonical translation in brain tissue [Ribo-Seq]

Project description:Activity-dependent ribosome profiling reveals the landscape of canonical and non-canonical translation in brain tissue [Ribo-Seq]

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Activity-dependent ribosome profiling reveals the landscape of canonical and non-canonical translation in brain tissue [RIP-Seq]

Project description:Activity-dependent ribosome profiling reveals the landscape of canonical and non-canonical translation in brain tissue [RIP-Seq]

| PRJNA1416247 | ENA

Activity-dependent ribosome profiling reveals the landscape of canonical and non-canonical translation in brain tissue [Ribo and RNA-Seq]

Project description:Activity-dependent ribosome profiling reveals the landscape of canonical and non-canonical translation in brain tissue [Ribo and RNA-Seq]

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RACK1 depletion in the ribosome induces selective translation for non-canonical autophagy.

Project description:RACK1, which was first demonstrated as a substrate of PKCβ II, functions as a scaffold protein and associates with the 40S small ribosomal subunit. According to previous reports, ribosomal RACK1 was also suggested to control translation depending on the status in translating ribosome. We here show that RACK1 knockdown induces autophagy independent of upstream canonical factors such as Beclin1, Atg7 and Atg5/12 conjugates. We further report that RACK1 knockdown induces the association of mRNAs of LC3 and Bcl-xL with polysomes, indicating increased translation of these proteins. Therefore, we propose that the RACK1 depletion-induced autophagy is distinct from canonical autophagy. Finally, we confirm that cells expressing mutant RACK1 (RACK1R36D/K38E) defective in ribosome binding showed the same result as RACK1-knockdown cells. Altogether, our data clearly show that the depletion of ribosomal RACK1 alters the capacity of the ribosome to translate specific mRNAs, resulting in selective translation of mRNAs of genes for non-canonical autophagy induction.

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The ribosome profiling landscape of yeast reveals a high diversity in pervasive translation.

Project description:BackgroundPervasive translation is a widespread phenomenon that plays a critical role in the emergence of novel microproteins, but the diversity of translation patterns contributing to their generation remains unclear. Based on 54 ribosome profiling (Ribo-Seq) datasets, we investigated the yeast Ribo-Seq landscape using a representation framework that allows the comprehensive inventory and classification of the entire diversity of Ribo-Seq signals, including non-canonical ones.ResultsWe show that if coding regions occupy specific areas of the Ribo-Seq landscape, noncoding regions encompass a wide diversity of Ribo-Seq signals and, conversely, populate the entire landscape. Our results show that pervasive translation can, nevertheless, be associated with high specificity, with 1055 noncoding ORFs exhibiting canonical Ribo-Seq signals. Using mass spectrometry under standard conditions or proteasome inhibition with an in-house analysis protocol, we report 239 microproteins originating from noncoding ORFs that display canonical but also non-canonical Ribo-Seq signals. Each condition yields dozens of additional microprotein candidates with comparable translation properties, suggesting a larger population of volatile microproteins that are challenging to detect. Our findings suggest that non-canonical translation signals may harbor valuable information and underscore the significance of considering them in proteogenomic studies. Finally, we show that the translation outcome of a noncoding ORF is primarily determined by the initiating codon and the codon distribution in its two alternative frames, rather than features indicative of functionality.ConclusionOur results enable us to propose a topology of a species' Ribo-Seq landscape, opening the way to comparative analyses of this translation landscape under different conditions.

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A non-canonical pathway from cochlea to brain signals tissue-damaging noise.

Project description:Intense noise damages the cochlear organ of Corti, particularly the outer hair cells (OHCs) [1]; however, this epithelium is not innervated by nociceptors of somatosensory ganglia, which detect damage elsewhere in the body. The only sensory neurons innervating the organ of Corti originate from the spiral ganglion, roughly 95% of which innervate exclusively inner hair cells (IHCs) [2-4]. Upon sound stimulation, IHCs release glutamate to activate AMPA-type receptors on these myelinated type-I neurons, which carry the neuronal signals to the cochlear nucleus. The remaining spiral ganglion cells (type IIs) are unmyelinated and contact OHCs [2-4]. Their function is unknown. Using immunoreactivity to cFos, we documented neuronal activation in the brainstem of Vglut3(-/-) mice, in which the canonical auditory pathway (activation of type-I afferents by glutamate released from inner hair cells) is silenced [5, 6]. In these deaf mice, we found responses to noxious noise, which damages hair cells, but not to innocuous noise, in neurons of the cochlear nucleus, but not in the vestibular or trigeminal nuclei. This response originates in the cochlea and not in other areas also stimulated by intense noise (middle ear and vestibule) as it was absent in CD1 mice with selective cochlear degeneration but normal vestibular and somatosensory function. These data imply the existence of an alternative neuronal pathway from cochlea to brainstem that is activated by tissue-damaging noise and does not require glutamate release from IHCs. This detection of noise-induced tissue damage, possibly by type-II cochlear afferents, represents a novel form of sensation that we term auditory nociception.

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