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GLABRA2 transcription factor integrates arsenic tolerance with epidermal cell fate determination
Summary Arsenic poses a global threat to living organisms, compromising crop security and yield. Limited understanding of the transcriptional network integrating arsenic‐tolerance mechanisms with plant developmental responses hinders the development of strategies against this toxic metalloid. Here,...
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Published in: | The New phytologist 2024-12, Vol.244 (5), p.1882-1900 |
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Main Authors: | , , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | Summary
Arsenic poses a global threat to living organisms, compromising crop security and yield. Limited understanding of the transcriptional network integrating arsenic‐tolerance mechanisms with plant developmental responses hinders the development of strategies against this toxic metalloid.
Here, we conducted a high‐throughput yeast one‐hybrid assay using as baits the promoter region from the arsenic‐inducible genes ARQ1 and ASK18 from Arabidopsis thaliana, coupled with a transcriptomic analysis, to uncover novel transcriptional regulators of the arsenic response.
We identified the GLABRA2 (GL2) transcription factor as a novel regulator of arsenic tolerance, revealing a wider regulatory role beyond its established function as a repressor of root hair formation. Furthermore, we found that ANTHOCYANINLESS2 (ANL2), a GL2 subfamily member, acts redundantly with this transcription factor in the regulation of arsenic signaling. Both transcription factors act as repressors of arsenic response. gl2 and anl2 mutants exhibit enhanced tolerance and reduced arsenic accumulation. Transcriptional analysis in the gl2 mutant unveils potential regulators of arsenic tolerance.
These findings highlight GL2 and ANL2 as novel integrators of the arsenic response with developmental outcomes, offering insights for developing safer crops with reduced arsenic content and increased tolerance to this hazardous metalloid. |
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ISSN: | 0028-646X 1469-8137 1469-8137 |
DOI: | 10.1111/nph.20099 |