Boron modulates cell wall structure that alleviate aluminum toxicity-induced root growth defects in citrus

•HC1 is a vital binding site for Al in citrus root CW compared with pectin.•Boron regulates CW compounds via changing enzymes network to alleviate Al toxicity.•Boron supply reduced Al toxicity by decreasing Al accumulated in HC1 and pectin. Based on the soil acidification situation in citrus plantat...

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Veröffentlicht in:Scientia horticulturae 2024-07, Vol.333, p.113240, Article 113240
Hauptverfasser: Yan, Lei, Cheng, Jin, Riaz, Muhammad, Xiao, Siyun, Jiang, Cuncang
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Sprache:eng
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Zusammenfassung:•HC1 is a vital binding site for Al in citrus root CW compared with pectin.•Boron regulates CW compounds via changing enzymes network to alleviate Al toxicity.•Boron supply reduced Al toxicity by decreasing Al accumulated in HC1 and pectin. Based on the soil acidification situation in citrus plantation of southern China and even worldwide, it's essential to explore improved methods for resistant aluminum (Al) toxicity in plant. Trifoliate (Poncirus trifoliate (L) Raf.) is the most common rootstock in China. The ambition of this research was to illustrate the influence of boron (B) on Al bound in cell wall (CW) and the mechanism in trifoliate seedlings. Healthy seedlings were exposed to 0 or 300 µM AlCl3·6H2O with 10 µM B (H3BO3, control) and 50 µM B, respectively. The results displayed that Al accumulated in roots and root tips during Al exposure. However, Al content in root rips was reduced under B sufficient that reflected by lower morin fluorescence intensity compared to B10-treated roots. More specifically, B addition abates the Al content in root CW, manifested in lower Al content in pectin and hemicellulose 1 (HC1), with HC1 being more prominent. Moreover, B addition inhibited the pectin methyl-esterase (PME) activity to reduce pectin content, while increasing the xyloglucan endotransglucosylase (XET) and xyloglucan endotransglucosylase-hydrolase (XEH) activity. Thereby HC1 content was decreased, ultimately suppressing the bound site of Al in pectin and HC1, and diminished Al content in CW with B supply. Collectively, our results illustrate that B supply was attributed to the mitigation effect of B on Al toxicity by induced devaluation of Al accumulation in CW, which was associated with the reduction of binding Al with pectin and HC1 by regulating compounds of CW through adjusting CW enzymes (PME, XET, and XEH).
ISSN:0304-4238
1879-1018
DOI:10.1016/j.scienta.2024.113240