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Published on: March 30, 2018
MAPKs regulate root growth by influencing auxin signaling and cell cycle-related gene expression in cadmium-stressed
Feng Yun Zhao1, Fan Hu, Shi Yong Zhang
1College of Life Sciences, Shandong University of Technology, Zibo, 255049, Shandong Province, People's Republic of China. zhaofengyun@sdut.edu.cn
Abstract:
This work aims to analyze the relationship between root growth, mitogen-activated protein kinase (MAPK), auxin signaling, and cell cycle-related gene expression in cadmium (Cd)-stressed rice. The role of MAPKs in auxin signal modification and cell cycle-related gene expression during root growth was investigated by disrupting MAPK signaling using the MAPKK inhibitor PD98059 (PD). Treatment with Cd caused a significant accumulation of Cd in the roots. A Cd-specific probe showed that Cd is mainly localized in the meristematic zone and vascular tissues. Perturbation of MAPK signaling using PD significantly suppressed root system growth under Cd stress. The transcription of six MAPK genes was inhibited by Cd compared to the control. Detection using DR5-GUS transgenic rice showed that the intensity and distribution pattern of GUS staining was similar in roots treated with PD or Cd, whereas in Cd plus PD-treated roots, the GUS staining pattern was similar to that of the control, which indicates a close association of MAPK signaling with auxin homeostasis under control and Cd stress conditions. The expression of most key genes of auxin signaling, including OsYUCCA, OsPIN, OsARF, and OsIAA, and of most cell cycle-related genes, was negatively regulated by MAPKs under Cd stress. These results suggest that the MAPK pathway plays specific roles in auxin signal transduction and in the control of the cell cycle in response to Cd stress. Altogether, MAPKs take part in the regulation of root growth via auxin signal variation and the modified expression of cell cycle-related genes in Cd-stressed rice. A working model for the function of MAPKs in rice root systems grown under Cd stress is proposed.
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