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Gettemans, J.

Publications and source records attributed to Gettemans, J..

2 recordsLinked to original sources

TurboID proximity interactome mapping reveals NR2E3 association with AP-1 and retinal developmental complexes

The photoreceptor-specific nuclear receptor NR2E3 is a key transcription factor in the retinal transcriptional network, essential in photoreceptor cell fate and maintenance. Various biallelic loss-of-function variants lead to autosomal recessive inherited retinal disease (IRD), while a single missense variant G56R has been identified to cause autosomal dominant retinitis pigmentosa (adRP). However, a comprehensive understanding of the interactome of NR2E3 remains elusive. Here, we aimed to map the interactome of this nuclear receptor and the G56R pathogenic variant through proximity labelling followed by mass spectrometry. We used the TurboID "T2A split/link design" to identify the proximity interactome of wild-type NR2E3 and mutant G56R-NR2E3 in ARPE-19 cells. Several protein complexes involved in retinal development, including the AP-1 complex, were enriched. The results suggest similar interactomes for NR2E3 and G56R-NR2E3 in ARPE-19. However, BCOR was exclusively enriched in the G56R-NR2E3 network, strengthening the connection with the IRD phenotype. In conclusion, our approach has mapped the proximity interactome of NR2E3 and G56R-NR2E3, revealing interaction with protein complexes involved in (retinal) development.

systems biology↗

Nuclear fascin regulates cancer cell survival

Fascin is an important regulator of F-actin bundling leading to enhanced filopodia assembly. Fascin is also overexpressed in most solid tumours where it supports invasion through control of F-actin structures at the periphery and nuclear envelope. Recently fascin has been identified in the nucleus of a broad range of cell types but the contributions of nuclear fascin to cancer cell behaviour remain unknown. Here we demonstrate that fascin bundles F-actin within the nucleus to support chromatin organisation and efficient DNA damage response. Fascin associates directly with phosphorylated Histone H3 leading to regulated levels of nuclear fascin to support these phenotypes. Forcing nuclear fascin accumulation through the expression of nuclear-targeted fascin-specific nanobodies or inhibition of Histone H3 kinases results in enhanced and sustained nuclear F-actin bundling leading to reduced invasion, viability and nuclear fascin-specific/driven apoptosis. These findings represent an additional important route through which fascin can support tumorigenesis and provide insight into potential pathways for targeted fascin-dependent cancer cell killing.

cancer biology↗