Dynein light chain Dynlrb2 is essential for Murine leukemia virus traffic and nuclear entry.
Murine leukemia virus (MLV) requires the infected cell to divide to access the nucleus to integrate into the host genome. It has been determined that MLV uses the microtubule and actin network to reach the nucleus at the early stages of infection. Several studies have shown that viruses use the dynein motor protein associated with microtubules for their displacement. We have previously reported that Dynein light chain roadblock-type2 (Dynlrb2) knock-down significantly decreases MLV infection compared to non-silenced cells, suggesting a functional association between this dynein light chain and MLV preintegration complex (PIC). Here we aim to determine if the dynein complex Dynlrb2 subunit plays an essential role in the retrograde transport of MLV. For this, an MLV mutant containing the green fluorescent protein (GFP) fused to the viral protein p12 was used to assay the PIC localization and speed in cells were the expression of Dynlrb2 was modulated. We found a significant decrease in the arrival of MLV PIC to the nucleus and a reduced net speed of MLV PICs when Dynlrb2 was knocked down. On the contrary, an increase in nuclear localization is observed when Dynlrb2 is overexpressed. Our results suggest that Dynlrb2 plays an essential role in MLV retrograde transport. Importance Different viruses use different components of cytoplasmic dynein complex to traffic to their replication site. We have found that murine leukemia virus (MLV) depends on dynein light chain Dynlrb2 for infection, retrograde traffic and nuclear entry. Our study provides new information regarding the molecular requirements for retrograde transport of MLV preintegration complex and demonstrates the essential role of Dynlrb2 in MLV infection.