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Imprint
Molecular basis for nuclear egress of herpesviruses
Project
Project code: FLI-IMVZ-08-Ri-0552, 226088690
Contract period: 01.04.2017
- 31.08.2020
Purpose of research: Experimental development
Herpesvirus nucleocapsids are translocated from their assembly site in the nucleus to the cytosol by acquisition of a primary envelope at the inner nuclear membrane which subsequently fuses with the outer nuclear membrane. This vesicular transport of cargo through the nuclear envelope is unique in cell biology. It requires the presence of homologs of the conserved herpesviral pUL31 and pUL34 proteins which form the nuclear egress complex (NEC). The NEC recruits viral and cellular kinases to locally dissolve the nuclear lamina allowing access of nucleocapsids to the inner nuclear membrane and interaction with the NEC, which then drives primary envelopment. Although the general picture seems to be clear, the exact mechanism of nuclear egress is largely not understood. Thus, it is unclear what drives formation of primary envelopes, their fission and, in particular, their fusion with the outer nuclear membrane and whether this process includes not only viral but also cellular proteins. Moreover, we recently discovered that herpesvirus capsids are able to escape from the nucleus after induction of nuclear envelope breakdown (NEBD), a route which is not used under normal circumstances. Thus, in this project we want to elucidate molecular details of NEC formation and function, search for and identify cellular factors involved in this unique process and analyze which viral and cellular proteins are involved in NEBD or, in reverse, in maintenance of the integrity of the nucleus during herpesvirus infection.
Section overview
Subjects
- Animal health
- Biotechnology
Framework programme
Funding programme
Excutive institution
FLI - Institute of Molecular Virology and Cell Biology (FLI - IMVZ)
