Key message <p>Rice CC-BED NLR Xa1 recognizes TAL effectors through the interaction between ERF101 and TAL effectors<b>.</b></p> Abstract <p>The rice <i>Xa1</i> gene encodes a nucleotide-binding leucine-rich repeat receptor with an N-terminal coiled coil-zinc finger BED (CC-BED) domain. Xa1 recognizes the transcription activator-like (TAL) effectors of <i>Xanthomonas oryzae</i> pv. <i>oryzae</i> (<i>Xoo</i>) in the nucleus, triggering a number of immune responses, including hypersensitive cell death. We previously discovered that the rice transcription factor ERF101 directly interacts with Xa1, and functions as a positive regulator of Xa1-dependent immunity. However, the involvement of ERF101 in Xa1-induced immunity remains unclear. We herein demonstrated that the expression of the CC-BED domain in rice protoplasts inhibited Xa1-induced cell death. However, the CC-BED^C165A,C168A domain which has mutations of cysteine residues conserved in the zinc-finger motifs of BED domains and is essential for forming tetrahedral coordination geometry, failed to inhibit cell death or interact with ERF101. Therefore, Xa1-induced cell death appears to depend on the interaction between the BED domain and ERF101. In addition, we generated transgenic plants overexpressing N-terminal or C-terminal FLAG-tagged ERF101. <i>FLAG-ERF101</i> transgenic plants exhibited reduced levels of Xa1-mediated immunity against <i>Xoo</i>, even though the overexpression of <i>ERF101-FLAG</i> or non-tagged <i>ERF101</i> enhanced immunity. This result was consistent with the CC-BED domain interacting with C-terminal tagged ERF101, but not N-terminal tagged ERF101, whereas N-terminal and C-terminal tagged ERF101 both interacted with TAL effectors. Therefore, the interaction between the BED domain and ERF101 appears to be essential for the recognition of TAL effectors by Xa1.</p>