Abscisic acid (ABA) reduces accumulation of potentially toxic cadmium (Cd) in plants. How the ABA signal is transmitted to modulate Cd uptake remains largely unclear. Here, we report that the basic region/Leu zipper transcription factor ABSCISIC ACID-INSENSITIVE5 (ABI5), a central ABA signaling molecule, is involved in ABA-repressed Cd accumulation in plants by physically interacting with a previously uncharacterized R2R3-type MYB transcription factor, MYB49. Overexpression of the Cdinduced MYB49 gene in Arabidopsis (Arabidopsis thaliana) resulted in a significant increase in Cd accumulation, whereas myb49 knockout plants and plants expressing chimeric repressors of MYB49:ERF-associated amphiphilic repression motif repression domain (SRDX49) exhibited reduced accumulation of Cd. Further investigations revealed that MYB49 positively regulates the expression of the basic helix-loop-helix transcription factors bHLH38 and bHLH101 by directly binding to their promoters, leading to activation of IRON-REGULATED TRANSPORTER1, which encodes a metal transporter involved in Cd uptake. MYB49 also binds to the promoter regions of the heavy metal-associated isoprenylated plant proteins (HIPP22) and HIPP44, resulting in up-regulation of their expression and subsequent Cd accumulation. On the other hand, as a feedback mechanism to control Cd uptake and accumulation in plant cells, Cd-induced ABA up-regulates the expression of ABI5, whose protein product interacts with MYB49 and prevents its binding to the promoters of downstream genes, thereby reducing Cd accumulation. Our results provide new insights into the molecular feedback mechanisms underlying ABA signaling-controlled Cd uptake and accumulation in plants.

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Zinc oxide (ZnO) nanoparticles (nZnO) are among the most commonly used nanoparticles (NPs), and they have been shown to have harmful effects on plants. However, the molecular mechanisms underlying nZnO tolerance and root sensing of NP stresses have not been elucidated. Here, we compared the differential toxic effects of nZnO and Zn 2+ toxicity on plants during exposure and recovery using a combination of transcriptomic and physiological analyses. Although both nZnO and Zn 2+ inhibited primary root (PR) growth, nZnO had a stronger inhibitory effect on the growth of elongation zones, whereas Zn 2+ toxicity had a stronger toxic effect on meristem cells. Timely recovery from stresses is critical for plant survival. Despite the stronger inhibitory effect of nZnO on PR growth, nZnOexposed plants recovered from stress more rapidly than Zn 2+ -exposed plants upon transfer to normal conditions, and transcriptome data supported these results. In contrast to Zn 2+ toxicity, nZnO induced endocytosis and caused microfilament rearrangement in the epidermal cells of elongation zones, thereby repressing PR growth. nZnO also repressed PR growth by disrupting cell wall organization and structure through both physical interactions and transcriptional regulation. The present study provides new insight into the comprehensive understanding and re-evaluation of NP toxicity in plants.