Molecular mechanism of LEDGF/p75 dimerization

Vanda Lux 1, Tine Brouns 2, Kateřina Čermáková 1,3, Pavel Srb 1, Milan Fábry 4, Marcela Mádlíková 1, Magdalena Hořejší 4, Petr Novák 5, Michael Kugler 1, Jiří Brynda 1,4, Zeger Debyser 2, and Václav Veverka 1

1Institute of Organic Chemistry and Biochemistry of the CAS, Prague, Czech Republic

2KU Leuven, Molecular Virology and Gene Therapy, Leuven, Flanders, Belgium

3Department of Molecular & Cellular Biology, Center for Precision Environmental Health, and Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, USA

4Institute of Molecular Genetics of the CAS, Prague, Czech Republic

5Institute of Microbiology of the CAS, Prague, Czech Republic

6Department of Cell Biology, Faculty of Science, Charles University, Prague, Czech

vanda.lux@uochb.cas.cz


Protein dimerization of many eukaryotic transcription regulatory factors is critical for regulation of their functional complexes. Recently it was shown, that transcription regulatory role of an epigenetic reader Lens Epithelium Derived Growth Factor/p75 (LEDGF/p75, also known as PSIP1) requires at least two copies of this protein to overcome the nucleosome-induced barrier to transcription elongation. Moreover, various LEDGF/p75 binding partners are enriched for dimeric features further underscoring functional regulatory role of LEDGF/p75 dimerization. Here, we used a combination of biophysical and biochemical techniques to investigate the mechanism of LEDGF/p75 dimerization and its effect on molecular interactions with other proteins. We dissected the minimal dimerization region in the C-terminal part of LEDGF/p75 and with the help of paramagnetic NMR spectroscopy identified the key molecular contacts that were used to refine the solution structure of the dimer. The LEDGF/p75 dimeric assembly is stabilized by domain-swapping within the integrase binding domain and additional electrostatic ‘stapling’ of the negatively charged a-helix formed in the intrinsically disordered C-terminal region. We validated mechanism of dimer formation using structure-inspired dimerization defective LEDGF/p75 variants and chemical cross-linking coupled to mass spectrometry. We also show how dimerization might impact the LEDGF/p75 interactome.

This work was supported by grants from the GACR (grant No. 16-06357S to V.V )