| Two families of TIR domain containing proteins TIR-NBS (TN) and TIR-X (TX) that lack the atypical C-terminal leucine rich repeats (LRRs) were identified previously in the Arabidopsis Col-0 genome. My work focused on understanding the function of TX and TN family of proteins through the use of functional genomics approaches (including knockout and overexpression analyses). Transient overexpression of five TX and TN genes (AtTN3, AtTN10, AtTN11, AtTN21 and AtTX21) in tobacco led to the development of partial cell death responses characterized by the yellowing of tissue. The ability of the TX and TN genes to induce cell death responses upon transient expression was found to be dependent on enhanced disease resistance 1 (EDS1). The dependency of TN genes (AtTN3 ) on EDS1 to induce cell death was also found to be conserved in Arabidopsis. Arabidopsis stable overexpression transgenics of TX and TN genes resulted in the identification of variety of phenotypes involved with basal innate immune responses that are dependent on salicylic acid (SA). The interaction of the TN proteins (AtTN10) with chloroplastic proteins (phosphoglycerate dehydrogenase; 3PGDH), NBS-LRR proteins and other effector proteins suggests that TN proteins might act as guard complexes against pathogen effectors. |
