Effects of three auxin-inducible LBD members on lateral root formation in Arabidopsis thaliana

Effects of three auxin-inducible LBD members on lateral root formation in Arabidopsis thaliana
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三个生长素诱导的LBD成员对拟南芥侧根形成的影响

DOI:
10.1007/s00425-012-1673-3
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发表时间:
2012-10-01
期刊:
影响因子:
4.3
通讯作者:
Cui, Xianghuan
Cui, Xianghuan
中科院分区:
生物学2区
文献类型:
--
作者:
Feng, Zhenhua;Zhu, Jian;Cui, Xianghuan

文献摘要

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在拟南芥中,两种生长素反应因子(ARF 7和ARF 19)和几种Aux/IAAs调节生长素诱导的侧根(LR)形成。作为ARF 7和ARF 19的直接靶标,外侧器官边界结构域16(LBD 16)、LBD 29和LBD 18在侧根(LR)的形成中具有生物学功能。然而,这三个LBD的功能细节仍然不清楚。已显示每个单个T-DNA插入突变体具有比野生型略少的LR。然后,我们创建了一个三重突变体,它在LR形成中表现出显着的缺陷。我们的研究结果表明,lbd突变可以导致损害生长素诱导的周细胞分裂和一些D型细胞周期蛋白(CYCD)的表达水平。同时,PLETHORA(PLT)和PIN-形成(PIN),这已经被充分记录,以促进细胞有丝分裂活性和生长素反应的影响,所需的这些lbd突变下调。到目前为止,我们的研究结果表明,CYCD,PLT和PIN是LBD的主要目标。我们认为,这三个LBD参与细胞周期进程的周在响应生长素。这三个LBD基因中的任何一个在三重突变体中的过表达被发现不能完全取代其他两个LBD。lbd 29突变体的表型与lbd 16或lbd 18突变体不完全一致。这表明,LBD 29可能发挥独特的作用相比,LBD 16或LBD 18和LBD可能发挥部分独立的作用,在LRs的形成。
In Arabidopsis, two AUXIN RESPONSE FACTORs (ARF7 and ARF19) and several Aux/IAAs regulate auxin-induced lateral root (LR) formation. As direct targets of ARF7 and ARF19, LATERAL ORGAN BOUNDARIES DOMAIN 16 (LBD16), LBD29, and LBD18 have a biological function in the formation of lateral roots (LRs). However, the details of the functions of these three LBDs have remained unclear. Each single T-DNA insert mutant has been shown to have slightly fewer LRs than the wild type. We then created a triple mutant, which exhibited a dramatic defect in the LR formation. Our results show that the lbd mutations can lead to impairment in auxin-induced pericycle cell division and in the expression levels of some D-type cyclins (CYCDs). Simultaneously, PLETHORA (PLT) and PIN-FORMED (PIN), which have been well documented to promote cell mitotic activity and are required for auxin response effects, were down-regulated by these lbd mutations. Our results so far indicate that CYCDs, PLT, and PINs are the main targets of the LBDs. We believe that these three LBDs are involved in cell cycle progression of the pericycle in response to auxin. Overexpression of any of these three LBD genes in the triple mutant was found incapable of completely replacing the other two LBDs. The phenotypes of lbd29 mutants were not completely consistent with lbd16 or lbd18 mutants. This indicates that LBD29 may play a distinctive role compared with LBD16 or LBD18 and LBDs might play partially independent roles during the formation of LRs.