Mechanisms of inhibition of cadmium uptake and translocation by selenite: roles of root morphology, endogenous phytohormones, and root exudates via non–invasive micro–test technique and a combined analysis of transcriptome and metabolome

作者
Renwei Feng,Kongyuan Wu,Lizhen Wang,ZengFei Li,Jun Shen,ZiQing Liu,ZiHan Wu,ShengJie Shi,Hong Liu,Christopher Rensing
标识
DOI:10.22541/au.166902500.09665396/v1
摘要

Selenium (Se) can reduce the uptake and translocation of cadmium (Cd) in plants in a number of ways, including the regulation of root morphology. However, the actual mechanisms underlying the regulation of root morphology and root exudates by Se are unknown. To explore the action of Se in root systems, we investigated the effect of Se on root exudates, root morphology, root endogenous hormones, and Cd uptake using a non–invasive micro–test technique and a conjunction analysis of the transcriptome and metabolome in a hydroponically grown rice variety (Yong you No.9). The results showed that selenite (Se(IV)) significantly reduced Cd concentrations in the shoots and roots, and reduced Cd uptake efficiency in rice root hair. Additionally, compared to the 1 mg L Cd treatment (Cd1), treatment with 0.5 mg L Se(IV) and 1 mg L Cd (Se0.5Cd1) significantly reduced root surface area and root tip numbers, non–significantly reduced root length, and enhanced concentrations of auxin (IAA) and jasmonic acid (JA) in the roots. The results of metabolomic analysis showed that Se(IV) significantly increased the expression of differential metabolites correlated with the synthesis of IAA, JA, gibberellin (GA), and salicylic acid, such as GA53, M–SA, (+/–)7–epi–JA, and derivatives of tryptophan and indole. Analysis of the transcriptome indicated that no upregulated differentially expressed genes (DEGs) were enriched in IAA synthesis; however, some upregulated DEGs were found to be enriched in JA and GA53 synthesis pathways. In summary, although Se(IV) stimulated the synthesis of IAA, JA, and GA53, it significantly inhibited root growth mainly by 1) affecting the signal transduction of IAA and GA; 2) altering IAA polar transport and homeostasis; and 3) regulating the expression of the genes SAUR32, SAUR36, SAUR76, OsSub33, OsEXPA8, OsEXPA18, and Os6bglu24.

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