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. 1998 May 12;95(10):5655–5660. doi: 10.1073/pnas.95.10.5655

Figure 1.

Figure 1

atr1D regulatory phenotypes. (A) The trp1–100 atr1D double mutant is fluorescent on high-tryptophan medium. One-week-old seedlings of wild-type Col (TRP1/TRP1 ATR1/ATR1), Col trp1–100 gl1–1 (trp1/trp1 ATR1/ATR1), Col trp1–100 gl1–1 atr1D homozygotes (trp1/trp1 atr1D/atr1D), and Col trp1–100 gl1–1 atr1D/ATR1 F1 heterozygotes made by crossing Col trp1–100 gl1–1 atr1D with Col trp1–100 gl1–1 ATR1D (trp1/trp1 atr1D/ATR1) are shown under UV light grown on PNS medium containing 100 μM tryptophan. (B) The atr1D mutation confers dominant 5MT resistance. Seedlings of wild-type Col (ATR1/ATR1), a Col atr1D homozygote (atr1D/atr1D) made by crossing the Col trp1–100 atr1D isolate to Col and identifying homozygous 5MT-resistant plants, and a Col atr1D/ATR1 F1 heterozygote made by crossing Col atr1D with wild-type Col are shown after being grown on PNS medium containing 15 μM 5MT under yellow long-pass-filtered light for 10 days. (C) The atr1D mutation activates ASA1 expression in hypocotyls and lateral root junctions. Representative 2-week-old F1 seedlings of Arabidopsis made by crossing a transgenic No-O strain carrying the ASA1-GUS reporter fusion with either wild-type Col (ASA1-GUS/o ATR1/ATR1) or Col atr1D (ASA1-GUS/o atr1D/ATR1) are shown after growth on unsupplemented PNS medium followed by staining for GUS activity. Arrows indicate tissues with increased GUS expression in the atr1D mutant relative to the ATR1 control.