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. 2017 Mar 17;37(7):e00627-16. doi: 10.1128/MCB.00627-16

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Copyright © 2017 Roelants et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.

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FIG 7 — Fpk1 effects on both Akl1 and flippase function influence drug sensitivity. (A) Serial 10-fold dilutions of BY4741 (WT), akl1Δ (JTY6532), Fpk1^11A-expressing (YJW2), fpk1Δ fpk2Δ (YFR205), and dnf1Δ dnf2Δ dnf3Δ (PFY3272C) cells were spotted on plates lacking (−) or containing (+) doxorubicin (86 μM). The plates were scanned after incubation for 2 days at 30°C. (B) Same as in panel A, except with cells expressing Akl1-3×FLAG (YFR474-A), Akl1^AA-3×FLAG (YFR475-A), and Akl1^EE-3×FLAG (YFR476-A) and with a different stock of doxorubicin (which is light sensitive). (C) Serial 10-fold dilutions of akl1Δ (YFR479) cells carrying pRS315 (empty vector) or expressing from the same vector Akl1-3×FLAG (pFR316) or Akl1^AA-3×FLAG (pFR319) were spotted on plates lacking or containing hygromycin B (70 μM). The plates were scanned after incubation for 2 days at 30°C. (D) Serial 10-fold dilutions of akl1Δ (YFR479) cells carrying YCpUG (empty vector) or expressing from the GAL1 promoter GFP-Akl1 (pDD0938) or GFP-Akl1^AA (pFR303) were spotted on plates containing dextrose (Dex) or galactose (Gal), lacking or containing 0.8 μM myriocin (+Myr) as indicated. The plates were scanned after incubation for 3 days at 30°C.