Strader Lucia C, Monroe-Augustus Melanie, Rogers Kristen C, Lin Grace L, Bartel Bonnie
Department of Biochemistry and Cell Biology, Rice University, Houston, Texas 77005, USA.
Genetics. 2008 Dec;180(4):2019-31. doi: 10.1534/genetics.108.091512. Epub 2008 Oct 1.
Auxin controls numerous plant growth processes by directing cell division and expansion. Auxin-response mutants, including iba response5 (ibr5), exhibit a long root and decreased lateral root production in response to exogenous auxins. ibr5 also displays resistance to the phytohormone abscisic acid (ABA). We found that the sar3 suppressor of auxin resistant1 (axr1) mutant does not suppress ibr5 auxin-response defects, suggesting that screening for ibr5 suppressors might reveal new components important for phytohormone responsiveness. We identified two classes of Arabidopsis thaliana mutants that suppressed ibr5 resistance to indole-3-butyric acid (IBA): those with restored responses to both the auxin precursor IBA and the active auxin indole-3-acetic acid (IAA) and those with restored response to IBA but not IAA. Restored IAA sensitivity was accompanied by restored ABA responsiveness, whereas suppressors that remained IAA resistant also remained ABA resistant. Some suppressors restored sensitivity to both natural and synthetic auxins; others restored responsiveness only to auxin precursors. We used positional information to determine that one ibr5 suppressor carried a mutation in PLEIOTROPIC DRUG RESISTANCE9 (PDR9/ABCG37/At3g53480), which encodes an ATP-binding cassette transporter previously implicated in cellular efflux of the synthetic auxin 2,4-dichlorophenoxyacetic acid.
生长素通过指导细胞分裂和扩展来控制众多植物生长过程。生长素反应突变体,包括吲哚丁酸反应5(ibr5),对外源生长素表现出长根和侧根产生减少的现象。ibr5还表现出对植物激素脱落酸(ABA)的抗性。我们发现生长素抗性1(axr1)突变体的sar3抑制子不能抑制ibr5的生长素反应缺陷,这表明筛选ibr5抑制子可能会揭示对植物激素反应性重要的新组分。我们鉴定出两类抑制ibr5对吲哚-3-丁酸(IBA)抗性的拟南芥突变体:一类对生长素前体IBA和活性生长素吲哚-3-乙酸(IAA)的反应均恢复,另一类仅对IBA的反应恢复而对IAA的反应未恢复。IAA敏感性的恢复伴随着ABA反应性的恢复,而仍对IAA有抗性的抑制子对ABA也有抗性。一些抑制子对天然和合成生长素的敏感性均恢复;另一些仅对生长素前体恢复反应性。我们利用定位信息确定一个ibr5抑制子在多药抗性9(PDR9/ABCG37/At3g53480)中发生了突变,该基因编码一个ATP结合盒转运蛋白,之前已表明其参与合成生长素2,4-二氯苯氧乙酸的细胞外排。