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Excessive ammonium assimilation by plastidic glutamine synthetase causes ammonium toxicity in Arabidopsis thaliana

Plants use nitrate, ammonium, and organic nitrogen in the soil as nitrogen sources. Since the elevated CO 2 environment predicted for the near future will reduce nitrate utilization by C 3 species, ammonium is attracting great interest. However, abundant ammonium nutrition impairs growth, i.e., ammo...

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Published in:Nature communications 2021-08, Vol.12 (1), p.4944-4944, Article 4944
Main Authors: Hachiya, Takushi, Inaba, Jun, Wakazaki, Mayumi, Sato, Mayuko, Toyooka, Kiminori, Miyagi, Atsuko, Kawai-Yamada, Maki, Sugiura, Daisuke, Nakagawa, Tsuyoshi, Kiba, Takatoshi, Gojon, Alain, Sakakibara, Hitoshi
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Language:English
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Summary:Plants use nitrate, ammonium, and organic nitrogen in the soil as nitrogen sources. Since the elevated CO 2 environment predicted for the near future will reduce nitrate utilization by C 3 species, ammonium is attracting great interest. However, abundant ammonium nutrition impairs growth, i.e., ammonium toxicity, the primary cause of which remains to be determined. Here, we show that ammonium assimilation by GLUTAMINE SYNTHETASE 2 (GLN2) localized in the plastid rather than ammonium accumulation is a primary cause for toxicity, which challenges the textbook knowledge. With exposure to toxic levels of ammonium, the shoot GLN2 reaction produced an abundance of protons within cells, thereby elevating shoot acidity and stimulating expression of acidic stress-responsive genes. Application of an alkaline ammonia solution to the ammonium medium efficiently alleviated the ammonium toxicity with a concomitant reduction in shoot acidity. Consequently, we conclude that a primary cause of ammonium toxicity is acidic stress. Ammonium is an important nitrogen source for plants but excess ammonium impairs growth. Here the authors show that ammonium toxicity results from assimilation by GLUTAMINE SYNTHETASE 2 in the plastids which results in excess proton accumulation and acidity stress.
ISSN:2041-1723
2041-1723
DOI:10.1038/s41467-021-25238-7