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. Author manuscript; available in PMC: 2023 Jun 1.
Published in final edited form as: Nat Microbiol. 2022 Oct 31;7(12):1956–1966. doi: 10.1038/s41564-022-01243-4

Fig. 2: Absence of PhuZ causes mispositioning of the phage nucleus.

Fig. 2:

(A) Top: schematic of ΦKZ WT and phuZ::acrVIA1 (ΔphuZ) mutant genomes at the editing site. Bottom: Representative cells infected by WT (left) and ΔphuZ mutant (right). Phage DNA is stained by DAPI and shown as blue signals. The phage nucleus is mispositioned near the cell polar region upon infection by ΔphuZ, in contrast to the WT infection where the phage nucleus is centered. Scale bar denotes 2 μm. (B) Distribution of subcellular location of the phage nucleus in PAO1 cells infected by WT (blue, N = 521) and ΔphuZ (red, N = 503), and a PAO1 strain expressing wild-type PhuZ in trans (p-PhuZ) and infected by ΔphuZ (light green, N = 573). The diagram of an infected cell is shown on the top. The phage nucleus location is defined as the relative distance between the cell center and the nucleus center. (C) The phage nucleus location is plotted against the cell length for WT and ΔphuZ. The phage nucleus position in ΔphuZ-infected cells positively correlates with the cell length with a Pearson correlation coefficient of 0.486, p < 0.001 (two-sided), whereas there is no such correlation for WT infection with a Pearson correlation coefficient of 0.029, p = 0.505 (two-sided). (D) Efficiency of plating of WT and ΔphuZ on representative P. aeruginosa clinical strains. (The full panel of plaque assays is presented in Extended Data Fig. 4)