Summary Pollution of soil by the heavy metal cadmium (Cd) is a global environmental problem. The glutathione (GSH)‐dependent phytochelatin (PC) synthesis pathway is one of the most important mechanisms contributing to Cd accumulation and tolerance. However, the regulation of this pathway is poorly understood. Here, we identified an Arabidopsis thaliana cadmium‐tolerant dominant mutant xcd1‐D (XVE system‐induced cadmium‐tolerance 1) and cloned XCD1 gene (previously called MAN3), which encodes an endo‐β‐mannanase. Overexpression of MAN3 led to enhanced Cd accumulation and tolerance, whereas loss‐of‐function of MAN3 resulted in decreased Cd accumulation and tolerance. In the presence of estradiol, enhanced Cd accumulation and tolerance in xcd1‐D was associated with GSH‐dependent, Cd‐activated synthesis of PCs, which was correlated with coordinated activation of gene expression. Cd stress‐induced expression of MAN3 and the consequently increased mannanase activity, led to increased mannose content in cell walls. Moreover, mannose treatment not only rescued the Cd‐sensitive phenotype of the xcd1‐2 mutant, but also improved the Cd tolerance of wild‐type plants. Significantly, this mannose‐mediated Cd accumulation and tolerance is dependent on GSH‐dependent PC concentrations via coordinated control of expression of genes involved in PC synthesis. Our results suggest that MAN3 regulates the GSH‐dependent PC synthesis pathway that contributes to Cd accumulation and tolerance in A. thaliana by coordinated control of gene expression.

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Summary Controlled stability of proteins is a highly efficient mechanism to direct diverse processes in plants. A key regulatory system for protein stability is given by the CULLIN‐RING E3 ligases (CRLs). In this work, MYB43 is identified as a novel target of a CUL4‐DDB1‐PRL1 (PLEIOTROPIC REGULATORY LOCUS 1)‐RING E3 ligase (CRL4PRL1 E3 ligase). Its stability depends on the presence of PRL1, a WD40‐containing protein functioning as a substrate receptor of the CRL4 E3 ligases. Genetic studies have indicated that MYB43 is a negative regulator of cadmium (Cd) tolerance in Arabidopsis by transcriptional inhibition of important Cd transporters (HMA2, HMA3 and HMA4), while PRL1 and CUL4 positively regulate Cd tolerance. Expression of CUL4 and PRL1 was enhanced in response to Cd stress, and PRL1 can interact with and target MYB43 for degradation depending on assembly of CRL4PRL1 E3 ligase, and consequently increase the expression of HMA2, HMA3 and HMA4 through attenuating the transcriptional inhibition. HMA2 and HMA4 are shown to transport cadmium ion (Cd2+) from the roots of plants to the shoots through the xylem, ultimately increasing the plants’ tolerance to Cd stress.

Highlight PSE1 regulates Pb tolerance mainly through GSH-dependent phytochelatin synthesis by activating the expression of the genes involved in phytochelatin synthesis and at least partially through activating the expression of PDR12.

Potassium (K+) deficiency induces leaf senescence, and jasmonic acid (JA) plays a role in the regulation of leaf senescence; however, there is no direct evidence that JA has a role in the induction of leaf senescence by K+ deficiency. Here, we determined that JA is involved in the induction of leaf senescence by K+ deficiency. Leaf senescence was induced by K+ deficiency, as indicated by both the induction of expression of two senescence-associated genes, SAG12 and SAG13, and a decline in chlorophyll concentration; whereas inhibitors of JA biosynthesis, aspirin and salicylate, abolished the induction of leaf senescence by K+ deficiency. The JA concentration was threefold higher in the leaves of plants with K+ deficiency than it was in the leaves of control plants. In addition, transcript levels of two JA-responsive genes, PDF1.2 and Thi2.1, were higher in the leaves of plants with K+ deficiency than in the leaves of control plants. Our studies provide evidence that K+ deficiency induces leaf senescence, at least in part, via a JA-dependent pathway.