Involvement of G1-to-S transition and AhAUX-dependent auxin transport in abscisic acid-induced inhibition of lateral root primodia initiation in Arachis hypogaea L
文献类型： 外文期刊
作者： Guo, Dongliang 1 ; Liang, Jianhua 1 ; Qiao, Yanchun 3 ; Yan, Youchen 1 ; Li, Ling 1 ; Dai, Yanhong 1 ;
作者机构： 1.S China Normal Univ, Coll Life Sci, Guangdong Prov Key Lab Biotechnol Plant Dev, Guangzhou 510631, Guangdong, Peoples R China
2.Guangdong Acad Agr Sci, Inst Fruit Tree Res, Guangzhou 510641, Peoples R China
3.Guangzhou Acad Agr Sci, Guangzhou 510308, Guangdong, Peoples R China
关键词： Abscisic acid;Arachis hypogaea L;Lateral roots primordium;G1-to-S transition;AhAUX-dependent auxin transport
期刊名称：JOURNAL OF PLANT PHYSIOLOGY （ 影响因子：3.549； 五年影响因子：4.164 ）
ISSN： 0176-1617
年卷期： 2012 年 169 卷 11 期
页码：
收录情况： SCI
摘要： Previous study indicated that increasing endogenous abscisic acid (ABA) level could inhibit the lateral root (LR) formation of peanuts. In this study, we investigated the mechanisms by which ABA regulated lateral root primordia (LRP) initiation in peanuts (Arachis hypogaea L). Results suggested that ABA inhibited LRP initiation through blocking G1-to-S transition in seedlings and mature roots: e.g. 5.8% increase in the proportion of Cl phase and 18% decrease in the proportion of S phase after ABA treatment for 6 days. Further study of the expression of the cell cycle marker gene for G2-to-M transition in peanut roots suggested that AhCYCB1 expression was regulated by ABA. We also investigated the cooperative regulation of LRP initiation by ABA and indole-3-acetic acid (IAA). ABA treatment greatly reduced the effects of endogenous IAA on mature roots. The expression of the IAA polar transport gene AhAUX1 appeared to be regulated by ABA since ABA inhibited auxin-mediated LRP initiation by suppressing AhAUX-dependent auxin transport in peanut roots. We further examined the effect of ABA on the expression of DR5::GUS and AtAUX1 in the model plant Arabidopsis. The results of Arabidopsis were consistent with that of the peanut. (C) 2012 Elsevier GmbH. All rights reserved.
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