Anastasiia Lovchykova

All Publications

• Nonsense-mediated decay masks cryptic splicing events caused by TDP-43 loss. bioRxiv : the preprint server for biology Zeng, Y., Sianto, O., Lovchykova, A., Liu, C., Akiyama, T., Petrucelli, L., Gitler, A. D. 2025

  Abstract

  In frontotemporal dementia and amyotrophic lateral sclerosis, the RNA-binding protein TDP-43 is lost from the nucleus, leading to cryptic exon inclusion events in dozens of neuronal genes. Here, we show that many cryptic splicing events have been missed by standard RNA-sequencing analyses because they are substrates for nonsense-mediated decay. By inhibiting nonsense-mediated decay in neurons we unmask hundreds of novel cryptic splicing events caused by TDP-43 depletion, providing a new picture to TDP-43 loss of function in neurons.

  View details for DOI 10.1101/2025.07.09.664014

  View details for PubMedID 40672339

  View details for PubMedCentralID PMC12265704

• TDP-43 nuclear loss in FTD/ALS causes widespread alternative polyadenylation changes. bioRxiv : the preprint server for biology Zeng, Y., Lovchykova, A., Akiyama, T., Liu, C., Guo, C., Jawahar, V. M., Sianto, O., Calliari, A., Prudencio, M., Dickson, D. W., Petrucelli, L., Gitler, A. D. 2024

  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.

  View details for DOI 10.1101/2024.01.22.575730

  View details for PubMedID 38328059

  View details for PubMedCentralID PMC10849503