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. 2017 Dec 14;12(12):e0189694. doi: 10.1371/journal.pone.0189694

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© 2017 De San Eustaquio-Campillo et al

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig 1 — A. Schematic representation of the genetic organization of the B. subtilis ydcFGH locus. Gene size of the orfs and putative functions are indicated above each gene. “P_ydc lacZ” shows the approximate size and localization on the locus of the DNA fragment amplified to construct the transcriptional reporter fusion to lacZ (strain ABS1761). B. A P_ydc lacZ fusion is induced in a strain lacking mreB (3725 “ΔmreB”; ABS1762) but not mbl (Δmbl; ABS1769) nor in its wild type parent (Wt; ABS1761). C. Transformation of chromosomal DNA from strain ABS1761 (amyE::P_ydc lacZ-spc) into the recipient 3725 (neo- ΔmreB) leads to 100% of the spectinomycin/kanamycin resistant colonies expressing the lacZ reporter fusion (left) while the reverse transformation (right) leads to a limited number of blue colonies, indicating the absence of genetic link between ΔmreB and the factor inducing the reporter.