Novel Compounds Derived from DFPM Induce Root Growth Arrest through the Specific VICTR Alleles of Arabidopsis Accessions

Abstract

The small compound [5-(3,4-dichlorophenyl) furan-2-yl]-piperidine-1-ylmethanethione (DFPM) inhibits ABA responses by activating effector-triggered immune signal transduction in Arabidopsis. In addition to the known function of DFPM as an antagonist of ABA signaling, DFPM causes accession-specific root growth arrest in Arabidopsis Columbia-0 via the TIR-NLR protein VICTR (VARIATION IN COMPOUND TRIGGERED ROOT growth response) in an EDS1/PAD4/RAR1/SGT1B-dependent manner. Although DFPM could control the specific steps of various cellular responses, the functional residues for the activity of DFPM or the existence of a stronger version of DFPM modification have not been characterized thoroughly. This study analyzed twenty-two DFPM derivatives during root growth arrest, inhibition of ABA signaling, and induction of biotic signal transduction to determine critical residues that confer the specific activity of DFPM. Furthermore, this study identified two more Arabidopsis accessions that generate significant root growth arrest in response to DFPM derivatives dependent on multiple amino acid polymorphisms in the coding region of VICTR. The isolation of novel compounds, such as DFPM-5, and specific amino acid polymorphisms critical for the compound-induced responses will help determine the detailed regulatory mechanism for how DFPM regulates abiotic and biotic stress signaling interactions.