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Abstract Aluminum‐dependent stoppage of root growth requires the DNA damage response (DDR) pathway including the p53‐like transcription factor SUPPRESSOR OF GAMMA RADIATION 1 (SOG1), which promotes terminal differentiation of the root tip in response to Al dependent cell death. Transcriptomic analyses identified Al‐induced SOG1‐regulated targets as candidate mediators of this growth arrest. Analysis of these factors either as loss‐of‐function mutants or by overexpression in theals3‐1background shows ERF115, which is a key transcription factor that in other scenarios is rate‐limiting for damaged stem cell replenishment, instead participates in transition from an actively growing root to one that has terminally differentiated in response to Al toxicity. This is supported by a loss‐of‐functionerf115mutant raising the threshold of Al required to promote terminal differentiation of Al hypersensitiveals3‐1. Consistent with its key role in stoppage of root growth, a putativeERF115barley ortholog is also upregulated following Al exposure, suggesting a conserved role for this ATR‐dependent pathway in Al response. In contrast to other DNA damage agents, these results show that ERF115 and likely related family members are important determinants of terminal differentiation of the root tip following Al exposure and central outputs of the SOG1‐mediated pathway in Al response.
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RNA-binding protein MAC5A interacts with the 26S proteasome to regulate DNA damage response in Arabidopsis
Abstract DNA damage response (DDR) in eukaryotes is essential for the maintenance of genome integrity in challenging environments. The regulatory mechanisms of DDR have been well-established in yeast and humans. However, increasing evidence supports the idea that plants seem to employ different signaling pathways that remain largely unknown. Here, we report the role of MODIFIER OF SNC1, 4-ASSOCIATED COMPLEX SUBUNIT 5A (MAC5A) in DDR in Arabidopsis (Arabidopsis thaliana). Lack of MAC5A in mac5a mutants causes hypersensitive phenotypes to methyl methanesulfonate (MMS), a DNA damage inducer. Consistent with this observation, MAC5A can regulate alternative splicing of DDR genes to maintain the proper response to genotoxic stress. Interestingly, MAC5A interacts with the 26S proteasome (26SP) and is required for its proteasome activity. MAC core subunits are also involved in MMS-induced DDR. Moreover, we find that MAC5A, the MAC core subunits, and 26SP may act collaboratively to mediate high-boron-induced growth repression through DDR. Collectively, our findings uncover the crucial role of MAC in MMS-induced DDR in orchestrating growth and stress adaptation in plants.
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- Award ID(s):
- 1818082
- PAR ID:
- 10389085
- Publisher / Repository:
- Oxford University Press
- Date Published:
- Journal Name:
- Plant Physiology
- Volume:
- 191
- Issue:
- 1
- ISSN:
- 0032-0889
- Format(s):
- Medium: X Size: p. 446-462
- Size(s):
- p. 446-462
- Sponsoring Org:
- National Science Foundation
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