Fig. 1
From: TALE-induced immunity against the bacterial blight pathogen Xanthomonas oryzae pv. oryzae in rice
Working model of rice immunity triggered by transcription activator-like effectors (TALEs) and Xops of Xanthomonas oryzae pv. oryzae (Xoo), the causal agent of bacterial blight (BB) in rice. Rice may use executor (E) genes to trap TALEs, or the BED domain of NLR-A type proteins (e.g., XA1 and its alleles) to recognize TALEs, or NLR-B type proteins (e.g., XA47) to recognize unknown type-III secretion effectors (T3SEs) for effector-triggered immunity (ETI) against Xoo. On the other hand, Xoo evolves iTALE to suppress XA1-mediated resistance via an unknown TIP1 in rice. These ETIs may have connection with calcium (Ca2+) release and the burst of reactive oxygen species (ROS) for programmed cell death. Possibly, XA47 forms a resistosome like other coiled-coil NLR (CNL) proteins. Basically, Xoo secretes major virulence TALEs via the type-III secretion system (T3SS) to target the EBE (effector-binding element) of susceptibility (S) genes for ETS (effector-triggered susceptibility), and as a result to acquire nutrients from rice. This ETS may require unknown Xops to suppress PAMP-triggered immunity (PTI) via pattern-recognition receptors (PRR) on rice cell membrane. TALEs forms a complex with rice basic transcription factor OsTFIIAγ5 (Xa5) via a TFB domain to precisely activate the expression of E and S genes for ETI and ETS, respectively. If Xa5 mutated to xa5, the ETS turns to resistance by the loss of susceptibility (RLS). In addition, the disruption in EBEs of S genes makes rice acquire RLS. Xop, Xanthomonas outer protein; iTALE, interfering TALE; NLS, nuclear localization signals; AD, activation domain; TFB, transcription factor binding domain; TIP, TALE/iTALE interacting protein; NLR, nucleotide-binding leucine-rich repeat; CC, coiled-coil domain; BED, zinc-finger BED domain; NBS, nucleotide-binding site