Aluminum-Dependent Terminal Differentiation of the Arabidopsis Root Tip Is Mediated through an ATR-, ALT2-, and SOG1-Regulated Transcriptional Response.

By screening for suppressors of the aluminum (Al) hypersensitive Arabidopsis thaliana mutant als3-1, it was found that mutational loss of the Arabidopsis DNA damage response transcription factor SUPPRESSOR OF GAMMA RESPONSE1 (SOG1) confers increased Al tolerance similar to the loss-of-function mutants for the cell cycle checkpoint genes ATAXIA TELANGIECTASIA AND RAD3 RELATED (ATR) and ALUMINUM TOLERANT2 (ALT2). This suggests that Al-dependent terminal differentiation of the root tip is an active process resulting from activation of the DNA damage checkpoint by an ATR-regulated pathway, which functions at least in part through SOG1. Consistent with this, ATR can phosphorylate SOG1 in vitro. Analysis of SOG1's role in Al-dependent root growth inhibition shows that sog1-7 prevents Al-dependent quiescent center differentiation and endoreduplication in the primary root tip. Following Al exposure, SOG1 increases expression of several genes previously associated with DNA damage, including BRCA1 and with gel-shift analysis showing that SOG1 can physically associate with the BRCA1 promoter in vitro. Al-responsive expression of these SOG1-regulated genes requires ATR and ALT2, but not ATAXIA TELANGIECTASIA MUTATED, thus demonstrating that in response to chronic Al exposure, ATR, ALT2, and SOG1 function together to halt root growth and promote terminal differentiation at least in part in a transcription-dependent manner.

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