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. 2012 Nov 15;23(22):4402–4415. doi: 10.1091/mbc.E11-12-1015

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© 2012 Rockenbauch et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 2: — The TPRs are essential for the function of the ChAPs. (A) Chs3p-2GFP localized exclusively to internal structures in Δchs6, Chs6(ΔTPR1-4), and Chs6(ΔTPR5) strains. Accordingly, whereas calcofluor-stained wild-type cells showed bud scar chitin staining (arrowheads), this was absent in the mutants. Scale bar, 5 μm (B) Quantification of results in A. Graph shows an average of three experiments. Bud-neck staining was scored for the entire cell population in at least 100 cells per experiment. Bars, SD. (C) Chs6(ΔTPR1-4) and Chs6(ΔTPR5) strains were resistant to calcofluor. This defect was as pronounced as for a Δchs6 strain. The two mutant alleles showed no cross-complementation. Drop tests: plates were incubated at 30°C for 2–3 d. Blue, Chs6p alleles. Δ refers to Δchs6. (D) Bch2p requires TPRs for functionality. A CHS6 deletion in combination with a Δbch2, Bch2(ΔTPR1-4), or Bch2(ΔTPR5) allele led to lithium sensitivity. Drop tests were performed as described. Yellow, Bch2p alleles. Δ refers to Δchs6 and Δbch2, respectively. (D) Bch1p requires TPRs for functionality. Bch1(ΔTPR1-4) and Bch1(ΔTPR5) cells, like Δbch1, were sensitive to ammonium. Red, Bch1p alleles. Δ refers to Δbch1.