期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/ijms22115979
关键词
auxin transport; Calcium-Dependent Protein Kinase-Related Kinase (CRK); reactive oxygen species; superoxide anion; hydrogen peroxide; nitric oxide; paraquat; oxidative stress; root gravitropism; Arabidopsis
资金
- National Research, Development, and Innovation Office (NKFIH) [K124828, NN-118089, PD115502, PD128055, FK128920, K128728]
- Hungarian Ministry for National Economy [GINOP-2.3.2-15-2016-00001]
- Tempus Public Foundation, Hungary
- Biological Doctoral School University of Szeged, Hungary
The study reveals that Arabidopsis AtCRK5 protein kinase is involved in establishing the auxin gradient at root tips, and the delayed gravitropic response in the Atcrk5-1 mutant is associated with oxidative stress and nitric oxide levels. Treatment with oxidative stress inducers or H2O2 can partially restore proper auxin distribution.
The Arabidopsis AtCRK5 protein kinase is involved in the establishment of the proper auxin gradient in many developmental processes. Among others, the Atcrk5-1 mutant was reported to exhibit a delayed gravitropic response via compromised PIN2-mediated auxin transport at the root tip. Here, we report that this phenotype correlates with lower superoxide anion (O-2(center dot-)) and hydrogen peroxide (H2O2) levels but a higher nitric oxide (NO) content in the mutant root tips in comparison to the wild type (AtCol-0). The oxidative stress inducer paraquat (PQ) triggering formation of O-2(center dot-) (and consequently, H2O2) was able to rescue the gravitropic response of Atcrk5-1 roots. The direct application of H2O2 had the same effect. Under gravistimulation, correct auxin distribution was restored (at least partially) by PQ or H2O2 treatment in the mutant root tips. In agreement, the redistribution of the PIN2 auxin efflux carrier was similar in the gravistimulated PQ-treated mutant and untreated wild type roots. It was also found that PQ-treatment decreased the endogenous NO level at the root tip to normal levels. Furthermore, the mutant phenotype could be reverted by direct manipulation of the endogenous NO level using an NO scavenger (cPTIO). The potential involvement of AtCRK5 protein kinase in the control of auxin-ROS-NO-PIN2-auxin regulatory loop is discussed.
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