HCMV pUL135 remodels the actin cytoskeleton to impair immune recognition of infected cells.
Bottom Line: Without immune pressure, laboratory-adapted HCMV strains have undergone genetic alterations.Among these, the deletion of the UL/b' domain is associated with loss of virulence.An independent interaction between pUL135 and talin disrupted cell contacts with the extracellular matrix.
Affiliation: Institute of Infection & Immunity, Cardiff University School of Medicine, Heath Park, Cardiff CF14 4XN, UK. Electronic address: email@example.com.Show MeSH
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Mentions: Yeast two-hybrid assays and stable isotope labeling by amino acids in cell culture (SILAC) immunoprecipitation experiments were undertaken in order to identify pUL135-interacting partners. In the yeast two-hybrid screen, ABI1 and ABI2 were both identified in multiple clones. This finding was consolidated and expanded when SILAC immunoprecipitation experiments performed on pUL135-expressing fibroblasts identified WAVE2, ABI1, NAP1, CYFIP1, and talin-1 (Table S2). Significantly ABI1, ABI2, NAP1, CYFIP1, and WAVE2 itself are all components of the WAVE2 regulatory complex (WRC), which regulates the actin nucleator Arp2/3 (Takenawa and Suetsugu, 2007). The interaction with WAVE2, ABI1, ABI2, NAP1, CYFIP1, and talin-1 were validated in conventional immunoprecipitation experiments when pUL135 was expressed in both isolation and the context of HCMV infection (Figure 4A).
Affiliation: Institute of Infection & Immunity, Cardiff University School of Medicine, Heath Park, Cardiff CF14 4XN, UK. Electronic address: firstname.lastname@example.org.