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. 2015 Jun 2;6(3):e00531-15. doi: 10.1128/mBio.00531-15

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Copyright © 2015 Lev et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-ShareAlike 3.0 Unported license, which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original author and source are credited.

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FIG 2 — Spot dilution assays demonstrating a cell wall defect in the Δkcs1 and kinase-inactive Δkcs1::KCS1^AAA strains but not in the kinase-active Δkcs1::KCS1 strain. The strains were serially diluted 10-fold (10⁶ to 10 cells/spot from left to right) and spotted onto the test plates indicated. The dual nourseothricin (Nat) and neomycin (Neo) resistance of the Δkcs1::KCS1 and Δkcs1::KCS1^AAA strains confirms that integration of the KCS1 construct (providing Nat resistance) occurred in the Δkcs1 mutant strain background (Neo resistance).