Cellular and molecular insight into the inhibition of primary root growth of Arabidopsis induced by peptaibols, a class of linear peptide antibiotics mainly produced by Trichoderma spp.

Cellular and molecular insight into the inhibition of primary root growth of Arabidopsis induced by peptaibols, a class of linear peptide antibiotics mainly produced by Trichoderma spp.
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细胞和分子洞察 peptaibols 对拟南芥初生根生长的抑制作用,peptaibols 是一类主要由木霉属产生的线性肽抗生素。

DOI:
10.1093/jxb/erw023
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发表时间:
2016-04
影响因子:
6.9
通讯作者:
Song XY
Song XY
中科院分区:
生物学1区
文献类型:
--
作者:
Shi WL;Chen XL;Wang LX;Gong ZT;Li S;Li CL;Xie BB;Zhang W;Shi M;Li C;Zhang YZ;Song XY

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拟南芥根尖生长素稳态的破坏和随后木霉木霉毒素VI引起的根生长抑制中,JNK通道起着重要作用。 木霉菌是生产多种抗生素的众所周知的生物控制剂。肽类抗生素是一类主要由木霉产生的线性肽类抗生素。据报道,研究最多的peptaibol,在一定浓度下对植物有毒,但所涉及的机制尚不清楚。我们通过研究长枝木霉(Trichoderma longibrachiatum)SMF 2的一种肽素Trichokonin VI(TK VI)对拟南芥初生根的生长抑制作用来阐明肽素的毒性机制。TK VI通过抑制细胞分裂和细胞伸长,破坏根干细胞生态位维持来抑制根的生长。TK VI增加了根尖生长素含量,破坏了根尖生长素反应梯度。此外,我们筛选了拟南芥TK VI抗性突变体tkr 1。tkr 1在编码门控外向整流K+通道蛋白的BTK中具有点突变。这种突变缓解了TK VI诱导的抑制根中的K+外流,从而稳定了生长素梯度。tkr 1突变体也能抵抗丙甲霉素的植物毒性。我们的研究结果表明,peptaibol-植物的相互作用中发挥关键作用,有一个相互关系,peptaibol的peptaibol通道和生长素的稳态维持。细胞和分子的见解peptaibol诱导的植物根系生长的抑制推进我们的理解木霉-植物的相互作用。
GORK channels play an important role in the disruption of auxin homeostasis in Arabidopsis root tip and the subsequent inhibition of root growth caused by Trichokonin VI from Trichoderma. Trichoderma spp. are well known biocontrol agents that produce a variety of antibiotics. Peptaibols are a class of linear peptide antibiotics mainly produced by Trichoderma. Alamethicin, the most studied peptaibol, is reported as toxic to plants at certain concentrations, while the mechanisms involved are unclear. We illustrated the toxic mechanisms of peptaibols by studying the growth-inhibitory effect of Trichokonin VI (TK VI), a peptaibol from Trichoderma longibrachiatum SMF2, on Arabidopsis primary roots. TK VI inhibited root growth by suppressing cell division and cell elongation, and disrupting root stem cell niche maintenance. TK VI increased auxin content and disrupted auxin response gradients in root tips. Further, we screened the Arabidopsis TK VI-resistant mutant tkr1. tkr1 harbors a point mutation in GORK, which encodes gated outwardly rectifying K+ channel proteins. This mutation alleviated TK VI-induced suppression of K+ efflux in roots, thereby stabilizing the auxin gradient. The tkr1 mutant also resisted the phytotoxicity of alamethicin. Our results indicate that GORK channels play a key role in peptaibol–plant interaction and that there is an inter-relationship between GORK channels and maintenance of auxin homeostasis. The cellular and molecular insight into the peptaibol-induced inhibition of plant root growth advances our understanding of Trichoderma–plant interactions.