Key Laboratory of Tropical Plant Resources and Sustainable Use, Xishuangbanna Tropical Botanical Garden, Chinese Academy of Sciences Kunming, Yunnan 650223, China.
School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
J Exp Bot. 2017 Mar 1;68(7):1743-1755. doi: 10.1093/jxb/erx043.
Iron (Fe) deficiency is a limiting factor for the normal growth and development of plants, and many species have evolved sophisticated systems for adaptation to Fe-deficient environments. It is still unclear how plants sense Fe status and coordinate the expression of genes responsive to Fe deficiency. In this study, we show that the bHLH transcription factor bHLH115 is a positive regulator of the Fe-deficiency response. Loss-of-function of bHLH115 causes strong Fe-deficiency symptoms and alleviates expression of genes responsive to Fe deficiency, whereas its overexpression causes the opposite effect. Chromatin immunoprecipitation assays confirmed that bHLH115 binds to the promoters of the Fe-deficiency-responsive genes bHLH38/39/100/101 and POPEYE (PYE), which suggests redundant molecular functions with bHLH34, bHLH104, and bHLH105. This is further supported by the fact that the bhlh115-1 mutant was complemented by overexpression of any of bHLH34, bHLH104, bHLH105, and bHLH115. Further investigations determined that bHLH115 could interact with itself and with bHLH34, bHLH104, and bHLH105. Their differential tissue-specific expression patterns and the severe Fe deficiency symptoms of multiple mutants supported their non-redundant biological functions. Genetic analysis revealed that bHLH115 is negatively regulated by BRUTUS (BTS), an E3 ligase that can interact with bHLH115. Thus, bHLH115 plays key roles in the maintenance of Fe homeostasis in Arabidopsis thaliana.
铁（Fe）缺乏是植物正常生长和发育的限制因素，许多物种已经进化出复杂的系统来适应缺铁环境。目前仍不清楚植物如何感知 Fe 状态以及协调对 Fe 缺乏做出响应的基因表达。在这项研究中，我们表明 bHLH 转录因子 bHLH115 是 Fe 缺乏反应的正调控因子。bHLH115 的功能丧失导致强烈的 Fe 缺乏症状，并减轻了对 Fe 缺乏做出响应的基因的表达，而其过表达则产生相反的效果。染色质免疫沉淀试验证实，bHLH115 结合到 Fe 缺乏响应基因 bHLH38/39/100/101 和 POPEYE（PYE）的启动子上，这表明与 bHLH34、bHLH104 和 bHLH105 具有冗余的分子功能。bHLH115 突变体可以被 bHLH34、bHLH104、bHLH105 和 bHLH115 的过表达互补，这进一步证实了这一点。进一步的研究确定 bHLH115 可以与自身以及 bHLH34、bHLH104 和 bHLH105 相互作用。它们在不同组织中的特异性表达模式以及多个突变体的严重 Fe 缺乏症状支持了它们非冗余的生物学功能。遗传分析表明，bHLH115 受 E3 连接酶 BRUTUS（BTS）的负调控，BTS 可以与 bHLH115 相互作用。因此，bHLH115 在维持拟南芥铁稳态中起关键作用。
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