Characterization of nucleocytoplasmic shuttling and intracellular localization signals in Duck Enteritis Virus UL54

• Published in: Biochimie Vol. 127; pp. 86 - 94
• Main Authors: Liu, Chaoyue, Cheng, Anchun, Wang, Mingshu, Chen, Shun, Jia, Renyong, Zhu, Dekang, Liu, Mafeng, Sun, Kunfeng, Yang, Qiao, Chen, Xiaoyue
• Format: Journal Article
• Language: English
• Published: France Elsevier B.V 01.08.2016
• Subjects: Active Transport, Cell Nucleus; Amino Acid Sequence; Animals; Cell Line; Cell Nucleus - metabolism; DEV; Ducks - virology; Enteritis - virology; Herpes simplex virus 1; Nuclear export signal; Nuclear localization signal; Nuclear Localization Signals; Shuttling; UL54; Viral Proteins - chemistry; Viral Proteins - metabolism; LMB; UL54; DMEM; CHX; DEV; NLS; BAC; Nuclear localization signal; Shuttling; CRM1; NES; Nuclear export signal
• ISSN: 0300-9084; 1638-6183
• DOI: 10.1016/j.biochi.2016.05.003

Duck Enteritis virus (DEV) UL54 is a homolog of herpes simplex virus-1 (HSV-1) trafficking protein ICP27, which plays an essential role in infection. In this study, DEV UL54 shuttling between the nucleus and cytoplasm was verified with a heterokaryon assay. One predicted nuclear export sequence (NES) (339–348 aa) was shown to be functional and chromosomal region maintenance 1 (CRM1)-dependent; however, the insensitivity of UL54 to Leptomycin B (LMB) and NES mutation suggests that other mechanisms are responsible for the observed nuclear export. Next, three non-classical nuclear localization sequences (NLSs), referred to as NLS1 (105–122 aa), NLS2 (169–192 aa) and NLS3 (257–274 aa), were identified. Furthermore, a recombinant DEV with the UL54 NLSs deleted (DEV- UL54 mNLSs) was constructed and showed that UL54 NLSs moderately affected DEV growth. •Duck Enteritis Virus UL54 is a nucleoplasm shuttling protein.•Duck Enteritis Virus UL54 encodes a CRM-1-dependent NES, although the nucleus export of UL54 is CRM-1-independent.•Duck Enteritis Virus UL54 contains three functionally related NLSs that are important for DEV growth.