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首页> 外文期刊>The Plant Journal >The Arabidopsis transcription factor TCP9 modulates root architectural plasticity, reactive oxygen species-mediated processes, and tolerance to cyst nematode infections
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The Arabidopsis transcription factor TCP9 modulates root architectural plasticity, reactive oxygen species-mediated processes, and tolerance to cyst nematode infections

机译：拟南芥转录因子 TCP9 调节根部结构可塑性、活性氧介导的过程和对囊肿线虫感染的耐受性

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Infections by root-feeding nematodes have profound effects on root system architecture and consequently shoot growth of host plants. Plants harbor intraspecific variation in their growth responses to belowground biotic stresses by nematodes, but the underlying mechanisms are not well understood. Here, we show that the transcription factor TEOSINTE BRANCHED/CYCLOIDEA/PROLIFERATING CELL FACTOR-9 (TCP9) modulates root system architectural plasticity in Arabidopsis thaliana in response to infections by the endoparasitic cyst nematode Heterodera schachtii. Young seedlings of tcp9 knock-out mutants display a significantly weaker primary root growth inhibition response to cyst nematodes than wild-type Arabidopsis. In older plants, tcp9 reduces the impact of nematode infections on the emergence and growth of secondary roots. Importantly, the altered growth responses by tcp9 are most likely not caused by less biotic stress on the root system, because TCP9 does not affect the number of infections, nematode development, and size of the nematode-induced feeding structures. RNA-sequencing of nematode-infected roots of the tcp9 mutants revealed differential regulation of enzymes involved in reactive oxygen species (ROS) homeostasis and responses to oxidative stress. We also found that root and shoot growth of tcp9 mutants is less sensitive to exogenous hydrogen peroxide and that ROS accumulation in nematode infection sites in these mutants is reduced. Altogether, these observations demonstrate that TCP9 modulates the root system architectural plasticity to nematode infections via ROS-mediated processes. Our study further points at a novel regulatory mechanism contributing to the tolerance of plants to root-feeding nematodes by mitigating the impact of belowground biotic stresses.
机译：root-feeding线虫感染的深远对根系结构和影响因此拍摄宿主植物的生长。港的种内变异的增长对地下的生物胁迫的响应线虫,但潜在的机制很好理解。转录因子墨西哥类蜀黍支/ CYCLOIDEA FACTOR-9增殖细胞(TCP9)调节根系架构在拟南芥可塑性反应由endoparasitic囊肿线虫感染异皮线虫属schachtii。淘汰赛突变体显示明显较弱主要根系生长抑制囊肿比野生型拟南芥线虫。植物,tcp9降低线虫的影响感染的出现和增长二次根。响应由tcp9最有可能不是所致少压力对根系生物,因为TCP9并不影响感染的数量,线虫开发和规模nematode-induced喂养结构。RNA-sequencing nematode-infected根源的tcp9突变体显示微分调节酶参与活性氧(ROS)体内平衡和对氧化应激的反应。还发现,增长tcp9里生根发芽突变体对外源性氢不太敏感在线虫过氧化,活性氧积累在这些突变体降低感染的网站。总之,这些观察证明TCP9调节根系统架构可塑性线虫感染通过ROS-mediated流程。在一本小说导致监管机制植物root-feeding线虫的宽容通过减轻地下的生物的影响压力。

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