Ojeda-Rivera Jonathan Odilón, Oropeza-Aburto Araceli, Herrera-Estrella Luis
Laboratorio Nacional de Genómica para la Biodiversidad (UGA) del Centro de Investigación y de Estudios Avanzados del IPN, Irapuato, México.
Plant and Soil Science Department, Institute of Genomics for Crop Abiotic Stress Tolerance, Texas Tech University, Lubbock, TX, United States.
Front Plant Sci. 2020 Sep 29;11:01200. doi: 10.3389/fpls.2020.01200. eCollection 2020.
Acidic soils constrain plant growth and development in natural and agricultural ecosystems because of the combination of multiple stress factors including high levels of Fe, toxic levels of Al, low phosphate (Pi) availability and proton rhizotoxicity. The transcription factor SENSITIVE TO PROTON RHIZOTOXICITY (STOP1) has been reported to underlie root adaptation to low pH, Al toxicity and low Pi availability by activating the expression of genes involved in organic acid exudation, regulation of pH homeostasis, Al detoxification and root architecture remodeling in . However, the mechanisms by which STOP1 integrates these environmental signals to trigger adaptive responses to variable conditions in acidic soils remain to be unraveled. It is unknown whether STOP1 activates the expression of a single set of genes that enables root adaptation to acidic soils or multiple gene sets depending on the combination of different types of stress present in acidic soils. Previous transcriptomic studies of mutants and wild-type plants analyzed the effect of individual types of stress prevalent in acidic soils. An integrative study of the transcriptional regulation pathways that are activated by STOP1 under the combination of major stresses common in acidic soils is lacking. Using RNA-seq, we performed a transcriptional dissection of wild-type and root responses, individually or in combination, to toxic levels of Al, low Pi availability, low pH and Fe excess. We show that the level of STOP1 is post-transcriptionally and coordinately upregulated in the roots of seedlings exposed to single or combined stress factors. The accumulation of STOP1 correlates with the transcriptional activation of stress-specific and common gene sets that are activated in the roots of wild-type seedlings but not in . Our data indicate that perception of low Pi availability, low pH, Fe excess and Al toxicity converges at two levels STOP1 signaling: post-translationally through the regulation of STOP1 turnover, and transcriptionally, the activation of STOP1-dependent gene expression that enables the root to better adapt to abiotic stress factors present in acidic soils.
酸性土壤限制了自然和农业生态系统中植物的生长发育，这是多种胁迫因素共同作用的结果，包括高含量的铁、有毒水平的铝、低磷有效性以及质子根际毒性。据报道，质子根际毒性敏感转录因子（STOP1）通过激活参与有机酸分泌、pH稳态调节、铝解毒和根系结构重塑的基因表达，使根系适应低pH、铝毒性和低磷有效性。然而，STOP1整合这些环境信号以触发对酸性土壤中多变条件的适应性反应的机制仍有待阐明。尚不清楚STOP1是激活一组使根系适应酸性土壤的基因，还是根据酸性土壤中存在的不同类型胁迫的组合激活多组基因。先前对突变体和野生型植物的转录组学研究分析了酸性土壤中普遍存在的单一类型胁迫的影响。缺乏对酸性土壤中常见的主要胁迫组合下由STOP1激活的转录调控途径的综合研究。我们使用RNA测序技术，对野生型和突变体根系对铝毒性、低磷有效性、低pH和铁过量单独或组合处理的反应进行了转录剖析。我们发现，暴露于单一或组合胁迫因子的幼苗根系中，STOP1的水平在转录后被协同上调。STOP1的积累与野生型幼苗根系中激活的胁迫特异性和共同基因集的转录激活相关，但在突变体中则不然。我们的数据表明，对低磷有效性、低pH、铁过量和铝毒性的感知在两个水平上汇聚于STOP1信号传导：通过调节STOP1的周转在翻译后水平，以及通过激活依赖于STOP1的基因表达在转录水平，从而使根系能够更好地适应酸性土壤中存在的非生物胁迫因子。
