Abstract
Despite the essentiality of Mn in terrestrial plants, its excessive accumulation in plant tissues can cause growth defects, known as Mn toxicity. Mn toxicity can be classified into apoplastic and symplastic types depending on its onset. Symplastic Mn toxicity is hypothesised to be more critical for growth defects. However, details of the relationship between growth defects and symplastic Mn toxicity remain elusive. In this study, we aimed to elucidate the molecular mechanisms underlying symplastic Mn toxicity in rice plants. We found that under excess Mn conditions, CO2 assimilation was inhibited by stomatal closure, and both carbon anabolic and catabolic activities were decreased. In addition to stomatal dysfunction, stomatal and leaf anatomical development were also altered by excess Mn accumulation. Furthermore, indole acetic acid (IAA) concentration was decreased, and auxin-responsive gene expression analyses showed IAA-deficient symptoms in leaves due to excess Mn accumulation. These results suggest that excessive Mn accumulation causes IAA deficiency, and low IAA concentrations suppress plant growth by suppressing stomatal opening and leaf anatomical development for efficient CO2 assimilation in leaves.
Highlights
Despite the essentiality of Mn in terrestrial plants, its excessive accumulation in plant tissues can cause growth defects, known as Mn toxicity
The Mg, Zn, and Cu concentrations increased under Mn-toxic conditions (Fig. 2). These results demonstrated decreased growth and Mn toxicity symptoms accompanied by Mn accumulation in leaves grown under Mn-toxic conditions
The quantum yield of non-radiative energy loss [Y(NO)] differed between the control and Mn-toxic conditions under low light irradiance; this difference was masked under high light irradiance (Fig. 3i). These results showed that the photoprotective mechanisms in photosystem II (PSII) are robust, but the redox state in PSII can be perturbed under Mn toxicity
Summary
Despite the essentiality of Mn in terrestrial plants, its excessive accumulation in plant tissues can cause growth defects, known as Mn toxicity. To Mn toxicity, r espectively[14,15,16,17] In addition to these mechanisms, Mn-tolerant plants, such as Helianthus annuus L., use trichomes as Mn storage tissue to avoid an excessive increase in Mn concentration within c ells[10,11]. This mechanism depends on the plant species and is not a generalised strategy to prevent Mn toxicity[11]. Because PhȮ is regenerated to phenolics after the reaction with Mn2+, the continuous reactions of H2O2-production/consumption by PODs accumulate oxidised phenolics and oxidise Mn in the a poplast[19]
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