Ivanchenko Maria G, Muday Gloria K, Dubrovsky Joseph G
Department of Botany and Plant Pathology, 2082 Cordley Hall, Oregon State University, Corvallis, OR 97331, USA.
Plant J. 2008 Jul;55(2):335-47. doi: 10.1111/j.1365-313X.2008.03528.x. Epub 2008 Apr 24.
Plant root systems display considerable plasticity in response to endogenous and environmental signals. Auxin stimulates pericycle cells within elongating primary roots to enter de novo organogenesis, leading to the establishment of new lateral root meristems. Crosstalk between auxin and ethylene in root elongation has been demonstrated, but interactions between these hormones in root branching are not well characterized. We find that enhanced ethylene synthesis, resulting from the application of low concentrations of the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC), promotes the initiation of lateral root primordia. Treatment with higher doses of ACC strongly inhibits the ability of pericycle cells to initiate new lateral root primordia, but promotes the emergence of existing lateral root primordia: behaviour that is also seen in the eto1 mutation. These effects are correlated with decreased pericycle cell length and increased lateral root primordia cell width. When auxin is applied simultaneously with ACC, ACC is unable to prevent the auxin stimulation of lateral root formation in the root tissues formed prior to ACC exposure. However, in root tissues formed after transfer to ACC, in which elongation is reduced, auxin does not rescue the ethylene inhibition of primordia initiation, but instead increases it by several fold. Mutations that block auxin responses, slr1 and arf7 arf19, render initiation of lateral root primordia insensitive to the promoting effect of low ethylene levels, and mutations that inhibit ethylene-stimulated auxin biosynthesis, wei2 and wei7, reduce the inhibitory effect of higher ethylene levels, consistent with ethylene regulating root branching through interactions with auxin.
植物根系在响应内源性和环境信号时表现出相当大的可塑性。生长素刺激伸长的初生根中的中柱鞘细胞进入从头器官发生,从而导致新的侧根分生组织的建立。生长素和乙烯在根伸长过程中的相互作用已得到证实,但这些激素在根分支中的相互作用尚未得到充分表征。我们发现,低浓度乙烯前体1-氨基环丙烷-1-羧酸(ACC)的应用导致乙烯合成增强,促进侧根原基的起始。用更高剂量的ACC处理强烈抑制中柱鞘细胞起始新侧根原基的能力,但促进现有侧根原基的出现:这种行为在eto1突变体中也可见。这些效应与中柱鞘细胞长度的减少和侧根原基细胞宽度的增加相关。当生长素与ACC同时应用时,ACC无法阻止生长素对ACC暴露前形成的根组织中侧根形成的刺激。然而,在转移到ACC后形成的根组织中,伸长减少,生长素不能挽救乙烯对原基起始的抑制作用,反而使其增加几倍。阻断生长素反应的突变体slr1和arf7 arf19,使侧根原基的起始对低乙烯水平的促进作用不敏感,而抑制乙烯刺激的生长素生物合成的突变体wei2和wei7,降低了较高乙烯水平的抑制作用,这与乙烯通过与生长素相互作用调节根分支一致。