ABCG42 interacts with ASR1 to regulate cadmium transport, sequestration, and tolerance in wheat

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ABSTRACT Cadmium (Cd) contamination in farmland soils severely threatens wheat productivity and human health via food chain transmission. Although ATP-binding cassette (ABC) transporters are known to participate in heavy metal uptake and detoxification in plants, the genetic mechanisms coordinating Cd uptake, root retention and long-distance translocation in wheat remain poorly understood. In this study, we identified the wheat ABC transporter ABCG42 as a key regulator of Cd bioaccumulation and partitioning by regulating cell wall sequestration and interacting with ABA-, stress- and ripening-induced protein 1 (ASR1). Knockout of ABCG42 reduced Cd retention in root cell walls, thereby decreasing root Cd uptake and root-to-shoot translocation. Conversely, ABCG42 overexpression enhanced Cd sequestration in root cell walls and reduced Cd translocation to shoots, revealing a dual role of ABCG42 in promoting root Cd uptake and limiting long-distance Cd transport. Unlike previously reported plasma‑membrane‑localized ABCG homologs that extrude Cd out of plant cells, this ER‑resident transporter facilitates root cell‑wall Cd sequestration. ABCG42 physically interacted with ASR1, and both proteins were co-localized to the endoplasmic reticulum (ER). ABCG42 overexpression upregulated ASR1 expression and increased abscisic acid (ABA), salicylic acid (SA), and gibberellic acid (GA) levels under Cd stress. Transcriptomic and proteomic analyses revealed that the ABCG42-ASR1 module modulates Cd tolerance by regulating hormone signaling, mitogen-activated protein kinase (MAPK) cascades, and antioxidant enzyme activity. Our findings elucidate a novel molecular module that integrates Cd transport and ABA signaling to coordinate wheat Cd tolerance and accumulation. Collectively, these findings establish ABCG42 as a key genetic determinant of wheat Cd uptake and partitioning, providing a mechanistic basis for developing genetic strategies to mitigate Cd accumulation and reduce Cd entry into the food chain.

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