TaRBP1 stabilizes TaGLTP and negatively regulates stripe rust resistance in wheat

Author:

Li Yue12,Zhang Rongrong12,Wu Yu12,Wu Qin12,Jiang Qiantao12,Ma Jian12,Zhang Yazhou12,Qi Pengfei12,Chen Guoyue12,Jiang Yunfeng12,Zheng Youliang12ORCID,Wei Yuming12,Xu Qiang12ORCID

Affiliation:

1. State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China Sichuan Agricultural University Chengdu China

2. Triticeae Research Institute, Sichuan Agricultural University Chengdu China

Abstract

AbstractThe dynamic balance and distribution of sphingolipid metabolites modulate the level of programmed cell death and plant defence. However, current knowledge is still limited regarding the molecular mechanism underlying the relationship between sphingolipid metabolism and plant defence. In this study, we identified a wheat RNA‐binding protein 1 (TaRBP1) and TaRBP1 mRNA accumulation significantly decreased in wheat after infection by Puccinia striiformis f. sp. tritici (Pst). Knockdown of TaRBP1 via virus‐induced gene silencing conferred strong resistance to Pst by enhancing host plant reactive oxygen species (ROS) accumulation and cell death, indicating that TaRBP1 may act as a negative regulator in response to Pst. TaRBP1 formed a homopolymer and interacted with TaRBP1 C‐terminus in plants. Additionally, TaRBP1 physically interacted with TaGLTP, a sphingosine transfer protein. Knockdown of TaGLTP enhanced wheat resistance to the virulent Pst CYR31. Sphingolipid metabolites showed a significant accumulation in TaGLTP‐silenced wheat and TaRBP1‐silenced wheat, respectively. In the presence of the TaRBP1 protein, TaGLTP failed to be degraded in a 26S proteasome‐dependent manner in plants. Our results reveal a novel susceptible mechanism by which a plant fine‐tunes its defence responses by stabilizing TaGLTP accumulation to suppress ROS and sphingolipid accumulation during Pst infection.

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

Plant Science,Soil Science,Agronomy and Crop Science,Molecular Biology

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