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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

Misexpression of AtTX12 encoding a Toll/Interleukin-1 receptor domain induces growth defects and expression of defense-related genes partially independently of EDS1 in Arabidopsis
Sang-Kee Song1,*
1Department of Biology, Chosun University
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.
Abstract, Accepted Manuscript(in press) [Submitted on October 24, 2016, Accepted on November 2, 2016]
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