NSR1/MYR2 is a negative regulator of ASN1 expression and its possible involvement in regulation of nitrogen reutilization in Arabidopsis
Autor: | Namie Ohtsuki, Toshitsugu Nakano, Yoshimi Nakano, Kaoru Suzuki, Yuki Naito |
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Rok vydání: | 2017 |
Předmět: |
0106 biological sciences
0301 basic medicine Senescence Nitrogen Photoperiod Asparagine synthetase Mutant Arabidopsis Plant Science Phloem Biology 01 natural sciences Negative regulator 03 medical and health sciences Genetics Transcription factor Vascular tissue Arabidopsis Proteins Aspartate-Ammonia Ligase Biological Transport General Medicine biology.organism_classification Plant Leaves 030104 developmental biology Biochemistry Agronomy and Crop Science Transcription Factors 010606 plant biology & botany |
Zdroj: | Plant Science. 263:219-225 |
ISSN: | 0168-9452 |
Popis: | Nitrogen (N) is a major macronutrient that is essential for plant growth. It is important for us to understand the key genes that are involved in the regulation of N utilization. In this study, we focused on a GARP-type transcription factor known as NSR1/MYR2, which has been reported to be induced under N-deficient conditions. Our results demonstrated that NSR1/MYR2 has a transcriptional repression activity and is specifically expressed in vascular tissues, especially in phloem throughout the plant under daily light-dark cycle regulation. The overexpression of NSR1/MYR2 delays nutrient starvation- and dark-triggered senescence in the mature leaves of excised whole aerial parts of Arabidopsis plants. Furthermore, the expression of asparagine synthetase 1 (ASN1), which plays an important role in N remobilization and reallocation, i.e. N reutilization, in Arabidopsis, is negatively regulated by NSR1/MYR2, since the expressions of NSR1/MYR2 and ASN1 were reciprocally regulated during the light-dark cycle and ASN1 expression was down-regulated in overexpressors of NSR1/MYR2 and up-regulated in T-DNA insertion mutants of NSR1/MYR2. Therefore, the present results suggest that NSR1/MYR2 plays a role in N reutilization as a negative regulator through controlling ASN1 expression. |
Databáze: | OpenAIRE |
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