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Nitrogen Source Dependent Changes in Central Sugar Metabolism Maintain Cell Wall Assembly in Mitochondrial Complex I-Defective frostbite1 and Secondarily Affect Programmed Cell Death

1
Institute of Experimental Plant Biology and Biotechnology, Faculty of Biology, University of Warsaw, I. Miecznikowa 1, 02-096 Warsaw, Poland
2
Umeå Plant Science Centre, Department of Plant Physiology, Umeå University, SE-90187 Umeå, Sweden, [email protected]
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(8), 2206; https://doi.org/10.3390/ijms19082206
Received: 11 June 2018 / Revised: 20 July 2018 / Accepted: 24 July 2018 / Published: 28 July 2018
(This article belongs to the Special Issue Plant Mitochondria)
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Abstract

For optimal plant growth, carbon and nitrogen availability needs to be tightly coordinated. Mitochondrial perturbations related to a defect in complex I in the Arabidopsis thalianafrostbite1 (fro1) mutant, carrying a point mutation in the 8-kD Fe-S subunit of NDUFS4 protein, alter aspects of fundamental carbon metabolism, which is manifested as stunted growth. During nitrate nutrition, fro1 plants showed a dominant sugar flux toward nitrogen assimilation and energy production, whereas cellulose integration in the cell wall was restricted. However, when cultured on NH4+ as the sole nitrogen source, which typically induces developmental disorders in plants (i.e., the ammonium toxicity syndrome), fro1 showed improved growth as compared to NO3 nourishing. Higher energy availability in fro1 plants was correlated with restored cell wall assembly during NH4+ growth. To determine the relationship between mitochondrial complex I disassembly and cell wall-related processes, aspects of cell wall integrity and sugar and reactive oxygen species signaling were analyzed in fro1 plants. The responses of fro1 plants to NH4+ treatment were consistent with the inhibition of a form of programmed cell death. Resistance of fro1 plants to NH4+ toxicity coincided with an absence of necrotic lesion in plant leaves. View Full-Text
Keywords: cell wall synthesis; complex I defect; frostbite1; mitochondrial mutant; NDUFS4; necrosis; sugar catabolism; sugar signaling; programmed cell death; reactive oxygen species cell wall synthesis; complex I defect; frostbite1; mitochondrial mutant; NDUFS4; necrosis; sugar catabolism; sugar signaling; programmed cell death; reactive oxygen species
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Podgórska, A.; Ostaszewska-Bugajska, M.; Tarnowska, A.; Burian, M.; Borysiuk, K.; Gardeström, P.; Szal, B. Nitrogen Source Dependent Changes in Central Sugar Metabolism Maintain Cell Wall Assembly in Mitochondrial Complex I-Defective frostbite1 and Secondarily Affect Programmed Cell Death. Int. J. Mol. Sci. 2018, 19, 2206.

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