The Rice TAL Effector–Dependent Resistance Protein XA10 Triggers Cell Death and Calcium Depletion in the Endoplasmic Reticulum

Dongsheng Tian(Temasek Life Sciences Laboratory), Junxia Wang(Temasek Life Sciences Laboratory), Xuan Zeng(Temasek Life Sciences Laboratory), Keyu Gu(Temasek Life Sciences Laboratory), Chengxiang Qiu(Temasek Life Sciences Laboratory), Xiaobei Yang(Temasek Life Sciences Laboratory), Zhiyun Zhou(Temasek Life Sciences Laboratory), Meiling Goh(Temasek Life Sciences Laboratory), Yanchang Luo(Temasek Life Sciences Laboratory), Maki Murata‐Hori(Temasek Life Sciences Laboratory), Frank F. White(Kansas State University), Zhongchao Yin(Temasek Life Sciences Laboratory)
The Plant Cell
January 1, 2014
Cited by 256Open Access
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Abstract

The recognition between disease resistance (R) genes in plants and their cognate avirulence (Avr) genes in pathogens can produce a hypersensitive response of localized programmed cell death. However, our knowledge of the early signaling events of the R gene-mediated hypersensitive response in plants remains limited. Here, we report the cloning and characterization of Xa10, a transcription activator-like (TAL) effector-dependent R gene for resistance to bacterial blight in rice (Oryza sativa). Xa10 contains a binding element for the TAL effector AvrXa10 (EBEAvrXa10) in its promoter, and AvrXa10 specifically induces Xa10 expression. Expression of Xa10 induces programmed cell death in rice, Nicotiana benthamiana, and mammalian HeLa cells. The Xa10 gene product XA10 localizes as hexamers in the endoplasmic reticulum (ER) and is associated with ER Ca(2+) depletion in plant and HeLa cells. XA10 variants that abolish programmed cell death and ER Ca(2+) depletion in N. benthamiana and HeLa cells also abolish disease resistance in rice. We propose that XA10 is an inducible, intrinsic terminator protein that triggers programmed cell death by a conserved mechanism involving disruption of the ER and cellular Ca(2+) homeostasis.


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