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. 2015 Jan 20;6(1):e02489-14. doi: 10.1128/mBio.02489-14

Correction for Sandai et al., The Evolutionary Rewiring of Ubiquitination Targets Has Reprogrammed the Regulation of Carbon Assimilation in the Pathogenic Yeast Candida albicans

Doblin Sandai 1,*, Zhikang Yin 1, Laura Selway 1, David Stead 1, Janet Walker 1, Michelle D Leach 1,*, Iryna Bohovych 1,*, Iuliana V Ene 1, Stavroula Kastora 1, Susan Budge 1, Carol A Munro 1, Frank C Odds 1, Neil A R Gow 1, Alistair J P Brown 1,
PMCID: PMC4313910  PMID: 25604791

AUTHOR CORRECTION

Volume 3, no. 6, doi:10.1128/mBio.00495-12, 2012. An error has been identified in Fig. 8B, where the wrong Western blot was used inadvertently. Figure 8B should appear as shown below. This change does not affect the conclusions in any way.

FIG 8 .

FIG 8 

Addition of a consensus ubiquitin site stimulates glucose-accelerated degradation of CaIcl1 in C. albicans. (B) The carboxy-terminal ubiquitination site from ScIcl1 was fused to CaIcl1 to create CaIcl1-Ubi-Myc in C. albicans DSC04 (Table S1). These cells were grown on lactate, and the levels of CaIcl1-Ubi-Myc were assayed by Western blotting after glucose addition. As controls, the stabilities of CaIcl1-Myc (CA1395; open diamonds) and ScIcl1-Myc (DSC01; gray squares) in C. albicans were compared under equivalent conditions. CaIcl1-Ubi-Myc, ScIcl1-Myc, and CaIcl1-Myc levels are expressed as a percentage of their abundance at time zero (100%). Similar data were obtained from two independent replicate experiments.


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