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Crosstalk between the nodulation signaling pathway and the autoregulation of nodulation in Medicago truncatula

机译:截短苜蓿中结瘤信号通路与结瘤自动调节之间的串扰

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摘要

P>A subset of CLAVATA3/endosperm-surrounding region-related (CLE) peptides are involved in autoregulation of nodulation (AON) in Medicago truncatula (e.g. MtCLE12 and MtCLE13). However, their linkage to other components of the AON pathways downstream of the shoot-derived inhibitor (SDI) is not understood.We have ectopically expressed the putative peptide ligand encoding genes MtCLE12 and MtCLE13 in M. truncatula which abolished nodulation completely in wild-type roots but not in the supernodulating null mutant sunn-4. Further, root growth inhibition was detected when MtCLE12 was ectopically expressed in wild-type roots or synthetic CLE12 peptide was applied exogenously.To identify downstream genes, roots of wild-type and sunn-4 mutant overexpressing MtCLE12 were used for quantitative gene expression analysis. We found that, in 35S:MtCLE12 roots, NODULE INCEPTION (NIN, a central regulator of nodulation) was down-regulated, whereas MtEFD (ethylene response factor required for nodule differentiation) and MtRR8 (a type-A response regulator thought to be involved in the negative regulation of cytokinin signaling), were up-regulated. Moreover, we found that the up-regulation of MtEFD and MtRR8 caused by overexpressing MtCLE12 is SUNN-dependent.Hence, our data link for the first time the pathways for Nod factor signaling, cytokinin perception and AON.
机译:P> CLAVATA3 /胚乳周围区域相关(CLE)肽的一个子集与截叶苜蓿(例如MtCLE12和MtCLE13)中的结瘤(AON)自动调节有关。然而,它们与芽衍生抑制剂(SDI)下游AON途径的其他组成部分之间的联系尚不清楚。我们已经在截短分枝杆菌中异位表达了推定的肽配体编码基因MtCLE12和MtCLE13,这完全消除了野生型结节根,但不在超结节的突变体sunn-4中。此外,当在野生型根中异位表达MtCLE12或外源应用合成的CLE12肽时,可检测到根生长抑制作用。为鉴定下游基因,使用野生型和sunn-4突变型过表达MtCLE12的根进行定量基因表达分析。我们发现,在35S:MtCLE12的根中,结节诱导(NIN,结瘤的中央调节剂)被下调,而MtEFD(结节分化所需的乙烯响应因子)和MtRR8(被认为与A型响应调节剂有关)在细胞分裂素信号转导的负调节中,被上调。此外,我们发现由过表达MtCLE12引起的MtEFD和MtRR8的上调是SUNN依赖性的。因此,我们的数据链接首次涉及Nod因子信号传导,细胞分裂素感知和AON的途径。

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