UC Riverside

Aluminum (Al) toxicity is a serious global problem that reduces crop production due to severe root growth inhibition. While Al toxic regions are considered to be some of the most biologically diverse areas of the world, most agriculturally relevant plants are derived from species that did not evolve natural mechanisms for Al exclusion or Al tolerance due to unconscious selection. There has been significant progress towards understanding the mechanisms for Al exclusion, but due to the numerous pathways and variety of molecular targets within the plant body that Al can interact with once internalized, Al tolerance is a particularly convoluted and evasive subject of study.

Several Al tolerant mutations have been identified through a suppressor mutagenesis approach using an Al hypersensitive mutant, als3-1. One of these suppressor mutations, sog1-7, was isolated and represents a mutation in SUPRESSOR OF GAMMA RESPONSE 1 (SOG1), a NAC domain containing transcription factor known to control cell cycle progression and entrance into endoreduplication in response to DNA damage. Loss of SOG1 fails to force differentiation of the quiescent center (QC) and halt root growth following Al exposure, indicating that is a required factor for active inhibition of root growth following exposure to Al. Furthermore, SOG1-mediated Al-dependent transcriptional responses are also dependent on two previously identified aluminum tolerance factor ATAXIA TELANGIECTASIA MUTATED AND RAD3-RELATED (ATR) and TANMEI/ALUMINUM TOLERANT 2 (ALT2) which are both implicated in DNA damage responses.

Another Al tolerant mutation was identified through the als3-1 suppressor mutagenesis with the isolation of suv2-3. This mutation represents an early stop codon in SENSITIVE TO UV2, whose wild type protein product is speculated to be the functional plant homologue to the mammalian ATR INTERACTING PROTEIN (ATRIP). SUV2 shuts down root growth through QC differentiation as part of the ATR- and SOG1- mediated transcriptional response to Al. These results show that Al promotes root growth inhibition through an ATR-, ALT2-, SOG1- and SUV2-dependent transcriptional response that induces a DNA damage response mechanism, ultimately resulting in QC differentiation and endoreduplication.