Significance of NatB-mediated N-terminal acetylation of auxin biosynthetic enzymes in maintaining auxin homeostasis in Arabidopsis thaliana

The auxin IAA (Indole-3-acetic acid) plays key roles in regulating plant growth and development, which depends on an intricate homeostasis that is determined by the balance between its biosynthesis, metabolism and transport. YUC flavin monooxygenases catalyze the rate-limiting step of auxin biosynth...

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Veröffentlicht in:Communications biology 2022-12, Vol.5 (1), p.1410-1410, Article 1410
Hauptverfasser: Liu, Hai-Qing, Pu, Zuo-Xian, Di, Dong-Wei, Zou, Ya-Jie, Guo, Yu-Man, Wang, Jun-Li, Zhang, Li, Tian, Peng, Fei, Qiong-Hui, Li, Xiao-Feng, Khaskheli, Allah Jurio, Wu, Lei, Guo, Guang-Qin
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Sprache:eng
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Zusammenfassung:The auxin IAA (Indole-3-acetic acid) plays key roles in regulating plant growth and development, which depends on an intricate homeostasis that is determined by the balance between its biosynthesis, metabolism and transport. YUC flavin monooxygenases catalyze the rate-limiting step of auxin biosynthesis via IPyA (indole pyruvic acid) and are critical targets in regulating auxin homeostasis. Despite of numerous reports on the transcriptional regulation of YUC genes, little is known about those at the post-translational protein level. Here, we show that loss of function of CKRC3/TCU2, the auxiliary subunit (Naa25) of Arabidopsis NatB, and/or of its catalytic subunit (Naa20), NBC, led to auxin-deficiency in plants. Experimental evidences show that CKRC3/TCU2 can interact with NBC to form a NatB complex, catalyzing the N-terminal acetylation (NTA) of YUC proteins for their intracellular stability to maintain normal auxin homeostasis in plants. Hence, our findings provide significantly new insight into the link between protein NTA and auxin biosynthesis in plants. CKRC3/TCU2 interacts with the NatB catalytic subunit to form a NatB complex, catalyzing the N-terminal acetylation of YUC proteins for their intracellular stability to maintain auxin homeostasis in plants.
ISSN:2399-3642
2399-3642
DOI:10.1038/s42003-022-04313-9