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Transposable Elements in Frontotemporal Lobar Degeneration

ABSTRACT: Transposable Elements in Frontotemporal Lobar Degeneration

PROVIDER: PRJNA561865 | ENA |

REPOSITORIES: ENA

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Transposable Elements in Frontotemporal Lobar Degeneration

Project description:Transposable Elements in Frontotemporal Lobar Degeneration

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TDP-43 forms amyloid filaments with a distinct fold in type A FTLD-TDP

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TDP-43 forms amyloid filaments with a distinct fold in type A FTLD-TDP

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Rescue of TDP-43 and neuronal pathologies by peripheral AAV-mediated expression of brain-penetrant progranulin in a mouse model of GRN-linked frontotemporal lobar degeneration

Project description:Progranulin (PGRN) haploinsufficiency is a major risk factor for Frontotemporal Lobar Degeneration with TDP-43 pathology (FTLD-TDP). Protein replacement therapeutic strategies are currently in clinical development, intended to restore PGRN levels in the central nervous system and slow or halt disease progression. However, such approaches require repeated dosing. Here, we explored the use of adeno-associated virus (AAV) to achieve sustained expression of a brain penetrant PGRN fusion protein, composed of a single chain variable fragment (scFv) recognizing mouse transferrin receptor (TfR) fused to human PGRN (AAV(L):bPGRN). We evaluated this approach for its ability to rescue pathological phenotypes in a double knockout mouse model lacking both PGRN and TMEM106b. A single administration of AAV(L):bPGRN reduced FTLD-TDP associated pathologies including severe motor function deficits, formation of insoluble, abnormally processed and phosphorylated TDP-43, as well as dysfunctional protein degradation, lipid dysregulation and gliosis.

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Transposable elements are co-opted as oncogenic regulatory elements by lineage-specific transcription factors in prostate cancer

Project description:Transposable elements hold regulatory functions to impact cell fate determination by controlling gene expression, which when altered can promote oncogenesis. Despite accounting for half of the human genome, little is known about the transcriptional mechanisms that confer regulatory properties to transposable elements in pluripotent, mature versus oncogenic cell states. Through positional analysis over repetitive DNA sequence of H3K27ac ChIP-seq from 32 different normal cell and tissue states, we report pluripotent stem and mature cell states-specific “regulatory transposable elements”. Those specific to pluripotent stem cells are binding sites for the pluripotency factors NANOG, SOX2 and OCT4. In mature cell and tissue states, regulatory transposable elements are docking sites for lineage-specific transcription factors, such as AR and FOXA1 in benign prostate epithelium. Expanding the positional analysis to localized prostate tumors, we show how cancer cell states remaining dependent on AR share regulatory transposable elements with pluripotent stem cells. These include regulatory transposable elements, such as Tigger3a, that serve as binding sites for AR and whose regulatory functions are required for prostate cancer cell growth. Together, our results suggest that oncogenesis differs from normal cell fate determination by hijacking pluripotent stem cells regulatory transposable elements that serve as docking sites for lineage-specific transcription factors.

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Epigenetic control of genes and transposable elements

Project description:Epigenetic control of genes and transposable elements

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Impact of transposable elements in Pleurotus ostreatus transcriptome profiles

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