RESUMEN
In China, saline-alkali lands constitute 5.01% of the total land area, having a significant impact on both domestic and international food production. Rapeseed (Brassica napus L.), as one of the most important oilseed crops in China, has garnered considerable attention due to its potential adaptability to saline conditions. Breeding and improving salt-tolerant varieties is a key strategy for the effective utilization of saline lands. Hence, it is important to conduct comprehensive research into the adaptability and salt tolerance mechanisms of Brassica napus in saline environments as well as to breed novel salt-tolerant varieties. This review summarizes the molecular mechanism of salt tolerance, physiological and phenotypic indexes, research strategies for the screening of salt-tolerant germplasm resources, and genetic engineering tools for salt stress in Brassica napus. It also introduces various agronomic strategies for applying exogenous substances to alleviate salt stress and provide technological tools and research directions for future research on salt tolerance in Brassica napus.
RESUMEN
Aluminum (Al) toxicity can seriously restrict crop production on acidic soils, which comprise 40% of the world's potentially arable land. The zinc finger transcription factor STOP1 has a conserved and essential function in mediating plant Al resistance. Al stress induces STOP1 accumulation via post-transcriptional regulatory mechanisms. However, the upstream signaling pathway involved in Al-triggered STOP1 accumulation remains unclear. Here, we report that the MEKK1-MKK1/2-MPK4 cascade positively regulates STOP1 phosphorylation and stability. Mutations of MEKK1, MKK1/2, or MPK4 lead to decreased STOP1 stability and Al resistance. Al stress induces the kinase activity of MPK4, which interacts with and phosphorylates STOP1. The phosphorylation of STOP1 reduces its interaction with the F-box protein RAE1 that mediates STOP1 degradation, thereby leading to enhanced STOP1 stability and Al resistance. Taken together, our results suggest that the MEKK1-MKK1/2-MPK4 cascade is important for Al signaling and confers Al resistance through phosphorylation-mediated enhancement of STOP1 accumulation in Arabidopsis.
Asunto(s)
Proteínas de Arabidopsis , Arabidopsis , Arabidopsis/metabolismo , Fosforilación , Aluminio , Proteínas de Arabidopsis/metabolismo , Sistema de Señalización de MAP Quinasas , Regulación de la Expresión Génica de las Plantas , Factores de Transcripción/metabolismoRESUMEN
The C2H2-type zinc finger transcription factor sensitive to proton rhizotoxicity 1 (STOP1) is crucial for aluminum (Al) resistance in Arabidopsis. The F-box protein Regulation of AtALMT1 Expression 1 (RAE1) was recently reported to regulate the stability of STOP1. There is a unique homolog of RAE1, RAH1 (RAE1 homolog 1), in Arabidopsis, but the biological function of RAH1 is still not known. In this study, we characterize the role of RAH1 and/or RAE1 in the regulation of Al resistance and plant growth. We demonstrate that RAH1 can directly interact with STOP1 and promote its ubiquitination and degradation. RAH1 is preferentially expressed in root caps and various vascular tissues, and its expression is induced by Al and controlled by STOP1. Mutation of RAH1 in rae1 but not the wild-type (WT) background increases the level of STOP1 protein, leading to increased expression of STOP1-regulated genes and enhanced Al resistance. Interestingly, the rah1rae1 double mutant shows reduced plant growth compared with the WT and single mutants under normal conditions, and introduction of stop1 mutation into the double mutant background can rescue its reduced plant growth phenotype. Our results thus reveal that RAH1 plays an unequally redundant role with RAE1 in the modulation of STOP1 stability and plant growth, and dynamic regulation of the STOP1 level is critical for the balance of Al resistance and normal plant growth.
Asunto(s)
Aluminio/toxicidad , Proteínas de Arabidopsis/metabolismo , Arabidopsis/fisiología , Proteínas F-Box/metabolismo , Proteínas de Complejo Poro Nuclear/metabolismo , Factores de Transcripción/metabolismo , Arabidopsis/genética , Arabidopsis/metabolismo , Proteínas de Arabidopsis/fisiología , Proteínas F-Box/fisiología , Regulación de la Expresión Génica de las Plantas , Proteínas de Complejo Poro Nuclear/fisiología , Estrés Fisiológico , Factores de Transcripción/fisiología , UbiquitinaciónRESUMEN
Aluminum (Al) toxicity is a major factor limiting crop production on acid soils, which represent over 30% of the world's arable land. Some plants have evolved mechanisms to detoxify Al. Arabidopsis, for example, secretes malate via the AtALMT1 transporter to chelate and detoxify Al. The C2H2-type transcription factor STOP1 plays a crucial role in Al resistance by inducing the expression of a set of genes, including AtALMT1 Here, we identify and characterize an F-box protein-encoding gene regulation of Atalmt1 expression 1 (RAE1) that regulates the level of STOP1. Mutation and overexpression of RAE1 increases or decreases the expression of AtALMT1 and other STOP1-regulated genes, respectively. RAE1 interacts with and promotes the degradation of STOP1 via the ubiquitin-26S proteasome pathway, while Al stress promotes the accumulation of STOP1. We find that STOP1 up-regulates RAE1 expression by directly binding to the RAE1 promoter, thus forming a negative feedback loop between STOP1 and RAE1. Our results demonstrate that RAE1 influences Al resistance through the ubiquitination and degradation of STOP1.