Overexpression of the ribosomal S30 subunit leads to indole-3-carbinol tolerance in Arabidopsis thaliana

Indole-3-carbinol (I3C), a hydrolysis product of indole-3-methylglucosinolate, is toxic to herbivorous insects and pathogens. In mammals, I3C is extensively studied for its properties in cancer prevention and treatment. Produced in Brassicaceae, I3C reversibly inhibits root elongation in a concentration-dependent manner. This inhibition is partially explained by the antagonistic action of I3C on auxin signaling through TIR1. To further elucidate the mode of action of I3C in plants, we have identified and characterized a novel Arabidopsis mutant tolerant to I3C, ICT1. This mutant was identified following screening of the Full-length cDNA Over-eXpression library (FOX) seed collection for root growth in the presence of exogenous I3C. ICT1 carries the AT2G19750 gene, which encodes an S30 ribosomal protein. Overexpression, but not knockout, of the S30 gene causes tolerance to I3C. The tolerance is specific to I3C, since ICT1 did not exhibit pronounced tolerance to other indole or benzoxazinoid molecules tested. ICT1 maintains I3C-induced antagonism of auxin signaling, indicating that the tolerance is due to an auxin-independent mechanism. Transcript profiling experiments revealed that ICT1 is transcriptionally primed to respond to I3C treatment.

Automated summary

The hydrolysis product of indole-3-methylglucosinolate, indole-3-carbinol (I3C), is toxic to herbivorous insects and pathogens, while extensively studied in mammals for its properties in cancer prevention and treatment. A novel Arabidopsis mutant, ICT1, has been identified to be tolerant to I3C, with the tolerance mechanism involving the S30 ribosomal protein. The tolerance is specific to I3C and maintained the antagonistic action of I3C on auxin signaling through an auxin-independent mechanism.