RPW8.1 and RPW8.2 share 45% identity and 65% similarity in amino acid sequences and confer broad-spectrum resistance against all tested infectious powdery mildew isolates in Arabidopsis ( Xiao et al., 2001). The Arabidopsis RESISTANCE TO POWDERY MILDE RPW8.1 ( RPW8.1) and RPW8.2 encode non-NLR R protein with a putative trans-membrane or signal peptide domain and one or two coiled-coil motifs ( Xiao et al., 2001 Wang et al., 2013). Barley Rpg1 encodes a receptor kinase-like protein with two tandem kinase domains conferring resistance to barley stem rust fungus ( Brueggeman et al., 2002). Wheat Lr34 encodes a putative ABC transporter protein conferring resistance to wheat rust and powdery mildew ( Krattinger et al., 2009). For example, tomato Pto encodes a serine-threonine protein kinase conferring resistance to Pseudomonas syringae pv. A few R genes encode atypical R proteins which are structurally different from the typical R proteins (NBS-LRRs and eLRRs), and mediate broad-spectrum and/or durable resistance to single or multiple pathogens. The R proteins can activate race-specific resistance via direct or indirect interaction with their cognate effectors ( Dodds et al., 2006 Krasileva et al., 2010). Most identified plant R genes encode proteins possessing an intracellular nucleotide-binding site and leucine-rich repeat (NBS-LRR) domain ( Bonardi et al., 2012) or an extracellular LRR (eLRR) domain ( Dangl and Jones, 2001). Defense responses in ETI are stronger than those in PTI and often culminate in hypersensitive response (HR) at the infection site ( Greenberg and Yao, 2004 Dangl et al., 2013). In turn, plants employ the second defense system, called effector-triggered immunity (ETI) that is activated upon recognition of pathogen effectors by plant intracellular nucleotide-binding and leucine-rich repeat receptors (NLRs) known as resistance (R) proteins ( Spoel and Dong, 2012 Dangl et al., 2013). However, adapted pathogens can subvert PTI by using virulent effectors ( Dou and Zhou, 2012).
#Timekeeper dead cells series#
PTI is featured by a series of defense responses, including burst of reactive oxygen species (ROS), deposition of callose, induction of defense–related genes ( Ebel and Mithöfer, 1998 Asai et al., 2002 Zipfel et al., 2006). The first system is termed pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI), which is activated when the receptors on the surface of host cells perceive conserved PAMPs ( Zipfel et al., 2006 Boller and Felix, 2009). To prevent the invasion of pathogenic microbes, plants have evolved two major defense systems in addition to pre-formed barriers such as cell walls and leaf hairs ( Jones and Dangl, 2006).
Taken together, these results indicate that XCT positively regulates RPW8.1-mediated cell death and disease resistance, and provide new insight into the regulatory mechanism of RPW8.1-mediated immunity. Consistently, the expression of RPW8.1 was down- and up-regulated in xct mutant and XCT overexpression lines, respectively. On the contrary, overexpression of XCT in R1Y4 background enhanced RPW8.1-mediated cell death, H 2O 2 production and resistance against powdery mildew. Here we further showed that mutation or down-regulation of XCT by artificial microRNA reduced RPW8.1-mediated immunity in R1Y4, a transgenic line expressing RPW8.1-YFP from the RPW8.1 native promoter. XCT has previously been identified as a circadian clock gene required for small RNA biogenesis and acting down-stream of ETHYLENE-INSENSITIVE3 ( EIN3) in the ethylene-signaling pathway. Map-based cloning identified a G-to-A point mutation at the 3′ splice site of the 8th intron, which resulted in splice shift to 8-bp down-stream of the original splice site of XCT in b3-17, and introduced into a stop codon after two codons leading to a truncated XCT. Forward genetic screen identified the b3-17 mutant that exhibited less cell death and susceptibility to powdery mildew and bacterial pathogens. Here, we report that XAP5 CIRCADIAN TIMEKEEPER ( XCT, At2g21150) positively regulates RPW8.1-mediated cell death and disease resistance.
However, the underlying regulatory mechanism remains largely elusive.
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