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Ageing-associated long non-coding RNA extends lifespan and reduces translation in non-dividing cells [aal1_ChIRP-RNAseq]

ABSTRACT: Ageing-associated long non-coding RNA extends lifespan and reduces translation in non-dividing cells [aal1_ChIRP-RNAseq]

PROVIDER: PRJNA1016262 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26048948_1.fastq.gz	Fastqsanger.gz
	SRR26048948_2.fastq.gz	Fastqsanger.gz
	SRR26048949_1.fastq.gz	Fastqsanger.gz
	SRR26048949_2.fastq.gz	Fastqsanger.gz
	SRR26048950_1.fastq.gz	Fastqsanger.gz

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Ageing-associated long non-coding RNA extends lifespan and reduces translation in non-dividing cells

Project description:Ageing-associated long non-coding RNA extends lifespan and reduces translation in non-dividing cells

| PRJNA1016255 | ENA

Ageing-associated long non-coding RNA extends lifespan and reduces translation in non-dividing cells [aal1OE_RNAseq]

Project description:Genomes pervasively produce long non-coding RNAs (lncRNAs) of largely unknown functions. Some of these lncRNAs have been implicated in roles related to ageing and associated diseases. Here we characterize aal1 (ageing-associated lncRNA 1) which is induced in non-dividing, ageing cells of fission yeast. Deletion of aal1 shortens the chronological lifespan of non-dividing cells, while ectopic overexpression of aal1 from a plasmid prolongs their lifespan, indicating that this lncRNA acts in trans. We find that aal1 genetically interacts with coding genes functioning in processes related to protein translation, and aal1 overexpression leads to repression of ribosomal protein genes and inhibition of cell growth. The aal1 RNA localizes to the cytoplasm and associates with ribosomes. Notably, aal1 deletion or overexpression is sufficient to increase or decrease the cellular ribosome content, respectively. We identify the mRNA rpl1901, encoding a ribosomal protein, as a binding target of aal1. The expression of rpl1901 is moderately repressed by aal1, and such moderate repression is critical and sufficient to extend the chronological lifespan. Remarkably, expression of the yeast aal1 lncRNA in the fly gut triggers a significant extension of the lifespan in flies. Based on these findings, we propose that the aal1 RNA can reduce the ribosome content by decreasing the levels of the Rpl1901 ribosomal protein, thus attenuating protein translation and promoting longevity. Although the aal1 lncRNA itself is not conserved, its effects in the fly raise the possibility that other organisms feature related mechanisms involving conserved ribosome-associated processes to control ageing.

2024-10-21 | GSE243034 | GEO

Ageing-associated long non-coding RNA extends lifespan and reduces translation in non-dividing cells [aal1OE_RNAseq]

Project description:Ageing-associated long non-coding RNA extends lifespan and reduces translation in non-dividing cells [aal1OE_RNAseq]

| PRJNA1016254 | ENA

Ageing-associated long non-coding RNA extends lifespan and reduces translation in non-dividing cells [aal1_ChIRP-RNAseq]

2024-10-21 | GSE243035 | GEO

Ageing-associated long non-coding RNA extends lifespan and reduces translation in non-dividing cells

Project description:Genomes produce widespread long non-coding RNAs (lncRNAs) of largely unknown functions. We characterize aal1 (ageing-associated lncRNA), which is induced in quiescent fission yeast cells. Deletion of aal1 shortens the chronological lifespan of non-dividing cells, while ectopic overexpression prolongs their lifespan, indicating that aal1 acts in trans. Overexpression of aal1 represses ribosomal-protein gene expression and inhibits cell growth, and aal1 genetically interacts with coding genes functioning in protein translation. The aal1 lncRNA localizes to the cytoplasm and associates with ribosomes. Notably, aal1 overexpression decreases the cellular ribosome content and inhibits protein translation. The aal1 lncRNA binds to the rpl1901 mRNA, encoding a ribosomal protein. The rpl1901 levels are reduced ~2-fold by aal1, which is sufficient to extend lifespan. Remarkably, the expression of the aal1 lncRNA in Drosophila boosts fly lifespan. We propose that aal1 reduces the ribosome content by decreasing Rpl1901 levels, thus attenuating the translational capacity and promoting longevity. Although aal1 is not conserved, its effect in flies suggests that animals feature related mechanisms that modulate ageing, based on the conserved translational machinery.

| S-SCDT-10_1038-S44319-024-00265-9 | biostudies-other

Boosting ATM activity alleviates ageing and extends lifespan in a mouse model of progeria.

Project description:Boosting ATM activity alleviates ageing and extends lifespan in a mouse model of progeria.

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Ageing-associated long non-coding RNA extends lifespan and reduces translation in non-dividing cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-10-21 | GSE243036 | GEO

Therapeutic reduction of rad23a extends lifespan and mitigates pathology in TDP-43 mice.

Project description:Therapeutic reduction of rad23a extends lifespan and mitigates pathology in TDP-43 mice. Xueshui Guo, Ravindra Prajapati, Jiyeon Chun, Insuk Byun, Kamil K Gebis, Yi-Zhi Wang, Karen Ling, Casey Dalton, Jeff Blair, Anahid Hamidianjahromi, Jeffrey N. Savas, Min Jae Lee, Jemeen Sreedharan, Robert Kalb

2024-07-12 | MSV000095320 | MassIVE

Identification of aal1 long non-coding RNA physically interacting proteins

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Ageing-dependent ribosome pausing and nascent polypeptide aggregation

Project description:Increased protein misfolding and aggregation are key hallmarks of ageing and many age-related diseases. As generating and maintaining a functional proteome (proteostasis) is crucial to every cellular process, this age-related decline in proteostasis is suggested to play a primary role in the breakdown of diverse cellular subsystems during ageing. Indeed, augmented proteostasis pathways are associated with extended lifespan across different species. With the ribosome as the earliest proteostasis checkpoint, decreased protein synthesis is also a conserved mechanism that extends lifespan. Yet, it remains unclear whether ageing impacts translation after initiation. Here, we use worms and yeast to investigate how ageing influences translation elongation. We show an age-dependent increase in ribosome pausing at diverse positions in coding sequences. This pausing is conserved in both worms and yeast, particularly at Arg and polybasic regions. We further show that such pausing is associated with the age-dependent aggregation of truncated nascent proteins involved in proteostasis pathways, notably aminoacyl tRNA synthetases. Moreover, we find that impairment in clearing truncated nascent proteins is associated with decreased lifespan. These data establish elongation kinetics and co-translational quality control as critical contributors of the age-related proteostasis collapse, which may precipitate the systemic decline observed during ageing.

2021-11-09 | GSE152850 | GEO

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