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. 2019 Jun 13;8:e46300. doi: 10.7554/eLife.46300

Figure 3. ALA-induced proteolysis depends on the N-terminal segment of GluTR1 and on GBP.

Figure 3.

(A) Schematic presentation of the constructs used to complement a hema1 knockout mutant. In addition to the full-length coding sequence of HEMA1, a construct coding for a truncated version of GluTR1 (ΔRED), which lacks 30 amino acids (aa) of the regulatory domain, was used to complement the hema1 mutant. Transgenes were under the control of the native HEMA1 promoter. TP, transit peptide. (B) GluTR1 content of 14-day-old Col-0, gbp-2, hema1/HEMA1, and hema1/ΔRED leaves incubated in buffer without (-) or with (+) 1 mM ALA for 24 hr in darkness. Signal intensities for GluTR1 are shown relative to the untreated WT (left) or the hema1/HEMA1 line (right). (C, D) Pchlide (C) and ncb heme content (D) of genotypes analyzed in (B) after 4 hr of treatment. Data are given as mean ± sd (n = 3). Letters indicate statistical groups determined by Student’s t-test (p<0.05).