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. Author manuscript; available in PMC: 2021 Oct 4.
Published in final edited form as: Cell Rep. 2020 Jul 28;32(4):107943. doi: 10.1016/j.celrep.2020.107943

Figure 7. Peroxisome Fragmentation during HCMV Infection Is Regulated by pUL37×1-Mediated Activation of PEX11β.

Figure 7.

(A) Images of peroxisomes (white, antibody against PEX14) from control cells (left), PEX11β KO CRISPR cells (middle), and control cells infected with ΔUL37 virus (right), before and after infection with HCMV. Infection is confirmed with an antibody against pUL99 (red). The peroxisome channel from three regions of interest is below each merged image. Scale bars represent 10 μm.

(B) For each condition in (A), peroxisome SA and SA:V was quantified (n > 20,000 peroxisomes in each condition). The SA:V schematic is shown to right, demonstrating the shift from spherical to flattened as the ratio increases. Box-and-whisker plots show whiskers at 10–90 percentiles, midline at median, and numerical value representing the mean. ***p < 0.001 compared to the wild-type mock-infected condition.

(C) Proposed model for the function of pUL37×1-PEX11β and MFF interactions, whereby pUL37×1 binds and activates PEX11β to promote peroxisome fission, generating fragmented peroxisomes (1). Alternatively, pUL37×1 is excluded from peroxisome membranes, likely by a currently unidentified host or viral factor, to form the enlarged and irregular peroxisomes (2).