Fig. 6: SFPQ re-distribution correlates with the temporal loss of H1.2 and H1.4 during EBV lytic reactivation.

a Immunoblot analysis of WCL from P3HR-1 cells at the indicated timepoints post EBV lytic reactivation by 4-HT addition. Representative immunoblot from n = 3 biological replicates and densitometry quantification with values normalized to the loading control GAPDH is shown. b Representative immunofluorescence images from n = 3 biological replicates of SFPQ (green), BZLF1 (magenta), or nuclear DAPI (blue) signals in P3HR-1 cells triggered for lytic reactivation by 4-HT for the indicated timepoints. Scale bar = 5 µm. c Quantification of the number of SFPQ puncta/nucleus during EBV lytic reactivation of cells treated as in (b). Violin plots show the median (solid line) and interquartile range (dotted lines). The number of nuclei quantified across three biological replicates are indicated. *p ≤ 0.05, **p ≤ 0.01, ****p ≤ 0.0001, ns not significant were calculated by one-way ANOVA. Values at a given timepoint were cross-compared with all subsequent timepoints. The color code indicated in the box at the top left indicates the timepoint used for cross-comparison for significance calculation. d Model of the roles of SFPQ and H1 in repressing EBV lytic reactivation. During EBV latency, SFPQ promotes expression of the histone H1 variants H1.2 and H1.4, which accumulate on the EBV genome at key regions and promote a compacted, repressive chromatin state that impedes expression of lytic genes. Upon EBV lytic reactivation, SFPQ is re-distributed within the nucleus to puncta by 6 h post lytic reactivation. This re-distribution precludes SFPQ from supporting H1.2 and H1.4 expression. Expression and protein levels of these H1 variants decline and so does their association with the EBV genome, which facilitates EBV lytic gene expression. Source data are provided as a Source Data file.