Ectopic expression of the Arabidopsis mutant L3 NB-LRR receptor gene in Nicotiana benthamiana cells leads to cell death.

Nucleotide-binding sites and leucine-rich repeat proteins (NLRs) act as critical intracellular immune receptors. Previous studies reported an Arabidopsis-resistant gene L3 (AT1G15890), which encoded a coiled-coil (CC) NLR that conferred cell death in bacteria; however, its function in planta remains unclear. This study describes a comprehensive structure-function analysis of L3 in Nicotiana benthamiana. The results of the transient assay showed that the L3 CC domain is sufficient for cell-death induction. The first 140 amino acid segment constituted the minimal function region that could cause cell death. The YFP-labeled L3 CC domain was localized to the plasma membrane, which was considered crucial for the function and self-interaction of the L3 CC domain. The results of point mutations analysis showed that L3 CC domain function is affected by mutations in some specific residues, and loss-of-function mutations in the CC domain affected the function of full-length L3. These study results offered considerable evidence to understand the activation mechanism of L3.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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