BZR1 Mediates Brassinosteroid-Induced Autophagy and Nitrogen Starvation in Tomato.

Plant Physiol

Department of Horticulture/Zhejiang Provincial Key Laboratory of Horticultural Plant Integrative Biology, Zhejiang University, Hangzhou 310058, China

Published: February 2019

Autophagy, an innate cellular destructive mechanism, plays crucial roles in plant development and responses to stress. Autophagy is known to be stimulated or suppressed by multiple molecular processes, but the role of phytohormone signaling in autophagy is unclear. Here, we demonstrate that the transcripts of autophagy-related genes () and the formation of autophagosomes are triggered by enhanced levels of brassinosteroid (BR). Furthermore, the BR-activated transcription factor brassinazole-resistant1 (BZR1), a positive regulator of the BR signaling pathway, is involved in BR-induced autophagy. Treatment with BR enhanced the formation of autophagosomes and the transcripts of in -overexpressing plants, while the effects of BR were compromised in -silenced plants. Yeast one-hybrid analysis and chromatin immunoprecipitation coupled with quantitative polymerase chain reaction revealed that BZR1 bound to the promoters of and The BR-induced formation of autophagosomes decreased in - and -silenced plants. Moreover, exogenous application of BR enhanced chlorophyll content and autophagosome formation and decreased the accumulation of ubiquitinated proteins under nitrogen starvation. Leaf chlorosis and chlorophyll degradation were exacerbated in -silenced plants and the BR biosynthetic mutant but were alleviated in - and -overexpressing plants under nitrogen starvation. Meanwhile, nitrogen starvation-induced expression of and autophagosome formation were compromised in both -silenced and plants but were increased in - and -overexpressing plants. Taken together, our results suggest that BZR1-dependent BR signaling up-regulates the expression of and autophagosome formation, which plays a critical role in the plant response to nitrogen starvation in tomato ().

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6426427PMC
http://dx.doi.org/10.1104/pp.18.01028DOI Listing

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