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<p>Several neurodegenerative disorders&#xa0;(NDDs), notably amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) are characterized by pathological cytoplasmic aggregation of TAR DNA-binding protein 43 (TDP-43) in neurons and glia. Primarily localized in the nucleus under physiological conditions, TDP-43 is a critical regulator of RNA processing and metabolism. Therefore, RNA changes induced by TDP-43 depletion or mutation could play an important role in the pathogenesis of ALS and other TDP-43 related NDDs.To investigate these effects in NSC34 motor neuron-like cells, a commonly used cellular model of ALS, we used RNA interference to knock down TDP-43 and overexpressed the ALS-associated TDP-43 M337V mutation. RNA from both these experiments was enriched for small and large transcripts and subsequently analyzed via next-generation sequencing.The resulting transcriptomics datasets offer a valuable resource for studying the impact of TDP-43 depletion and mutant over-expression in motor neurons. These data enable comprehensive differential expression analyses and functional enrichment studies, identifying cellular pathways affected by TDP-43 depletion or mutation. Additionally, the inclusion of non-coding RNAs facilitates the construction of gene regulatory networks, providing insights into the interplay between coding and non-coding RNAs in gene expression regulation under TDP-43 loss-of-function or pathogenic mutation conditions.</p>

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Coding and non-coding RNA expression in NSC34 cells following TDP-43 depletion and mutant TDP-43 M337V expression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月1日

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  • Ismail Gbadamosi,
  • Sandra Binias,
  • Bartłomiej Gielniewski,
  • Ramiro Magno,
  • Isabel Duarte,
  • Ali Jawaid

摘要

Several neurodegenerative disorders (NDDs), notably amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) are characterized by pathological cytoplasmic aggregation of TAR DNA-binding protein 43 (TDP-43) in neurons and glia. Primarily localized in the nucleus under physiological conditions, TDP-43 is a critical regulator of RNA processing and metabolism. Therefore, RNA changes induced by TDP-43 depletion or mutation could play an important role in the pathogenesis of ALS and other TDP-43 related NDDs.To investigate these effects in NSC34 motor neuron-like cells, a commonly used cellular model of ALS, we used RNA interference to knock down TDP-43 and overexpressed the ALS-associated TDP-43 M337V mutation. RNA from both these experiments was enriched for small and large transcripts and subsequently analyzed via next-generation sequencing.The resulting transcriptomics datasets offer a valuable resource for studying the impact of TDP-43 depletion and mutant over-expression in motor neurons. These data enable comprehensive differential expression analyses and functional enrichment studies, identifying cellular pathways affected by TDP-43 depletion or mutation. Additionally, the inclusion of non-coding RNAs facilitates the construction of gene regulatory networks, providing insights into the interplay between coding and non-coding RNAs in gene expression regulation under TDP-43 loss-of-function or pathogenic mutation conditions.