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. Author manuscript; available in PMC: 2018 Oct 5.
Published in final edited form as: Biochim Biophys Acta Gene Regul Mech. 2018 Oct 10;1861(10):952–961. doi: 10.1016/j.bbagrm.2018.08.006

Fig. 4. Suppression of NstADD toxicity by the cckA(L228P) mutant.

Fig. 4

(A) DIC and fluorescent micrographs of the extragenic suppressor mutant, ∆nstA cckA(L228P), harboring gfp-parB at the chromosomal xylX locus (xylX::Pxyl-gfp-parB). Red arrow-heads: cells with one GFP-ParB foci; white arrow-heads: cells with two partially segregated GFP-ParB foci. (B) DIC and fluorescent micrographs of ∆nstA cells expressing gfp-parB from xylX::Pxyl-gfp-parB. (C) Data representing the stalked cells with one (blue), two partially segregated (orange), normal bipolar (yellow), and multiple (grey) GFP-ParB foci in ∆nstA cckA(L228P) (data from 1032 stalked cells) or ∆nstA (data from 944 stalked cells). (D) DIC and fluorescent micrographs of WT cells harboring xylX::Pxyl-gfp-parB, and overexpressing NstADD from the vanillate inducible promoter (Pvan) on pBVMCS-4 or carrying the vector alone. The cells in (A), (B) and (D) were treated with 0.3% xylose to induce the production of GFP-ParB. Cells in (D) were additionally treated with 0.5 mM vanillate for 3 h to induce NstADD production. Scale bar in A, B and D: 2 μm.