To identify functions of uncharacterized genes in Arabidopsis, tissue-specific GAL4/UAS activation tags were introduced into the Q2610 enhancer trap line, highly active in post-embryonic roots, and a dominant mutant exhibiting stunted growth named defective root development 1-D (drd1-D) was isolated. The T-DNA tag was located within the promoter region of AtTX12, which is predicted to encode a truncated nucleotide-binding leucine-rich repeat (NLR) protein, containing a Toll/interleukin-1 receptor (TIR) domain. The transcripts of AtTX12 and defense-related genes were highly accumulated in drd1-D and the misexpression of AtTX12 by Q2610 recapitulated the drd1-D phenotypes. In the presence of ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1), a key transducer of signals triggered by TIR-type NLRs, a low-level AtTX12 misexpression induced strong defective phenotype such as seedling lethality whereas, in the absence of EDS1, a high-level AtTX12 misexpression induced weak growth defects like dwarfism suggesting that AtTX12 might function mainly EDS1-dependently and partially EDS1-independently as well.