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TDP-43 nuclear loss in FTD/ALS causes widespread alternative polyadenylation changes.

ABSTRACT: In frontotemporal dementia and amyotrophic lateral sclerosis, the RNA-binding protein TDP-43 is depleted from the nucleus. TDP-43 loss leads to cryptic exon inclusion but a role in other RNA processing events remains unresolved. Here, we show that loss of TDP-43 causes widespread changes in alternative polyadenylation, impacting expression of disease-relevant genes (e.g., ELP1, NEFL, and TMEM106B) and providing evidence that alternative polyadenylation is a new facet of TDP-43 pathology.

SUBMITTER: Zeng Y

PROVIDER: S-EPMC10849503 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature

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TDP-43 nuclear loss in FTD/ALS causes widespread alternative polyadenylation changes.

Zeng Yi Y Lovchykova Anastasiia A Akiyama Tetsuya T Liu Chang C Guo Caiwei C Jawahar Vidhya Maheswari VM Sianto Odilia O Calliari Anna A Prudencio Mercedes M Dickson Dennis W DW Petrucelli Leonard L Gitler Aaron D AD

bioRxiv : the preprint server for biology 20240122

In frontotemporal dementia and amyotrophic lateral sclerosis, the RNA-binding protein TDP-43 is depleted from the nucleus. TDP-43 loss leads to cryptic exon inclusion but a role in other RNA processing events remains unresolved. Here, we show that loss of TDP-43 causes widespread changes in alternative polyadenylation, impacting expression of disease-relevant genes (e.g., ELP1, NEFL, and TMEM106B) and providing evidence that alternative polyadenylation is a new facet of TDP-43 path ...[more]

PMID: 38328059

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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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