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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
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2018 (engelsk)Inngår i: International Journal of Molecular Sciences, ISSN 1422-0067, E-ISSN 1422-0067, Vol. 19, nr 8, artikkel-id 2206Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

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.

sted, utgiver, år, opplag, sider
MDPI, 2018. Vol. 19, nr 8, artikkel-id 2206
Emneord [en]
cell wall synthesis, complex I defect, frostbite1, mitochondrial mutant, NDUFS4, necrosis, sugar tabolism, sugar signaling, programmed cell death, reactive oxygen species
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Identifikatorer
URN: urn:nbn:se:umu:diva-152417DOI: 10.3390/ijms19082206ISI: 000442869800058PubMedID: 30060552OAI: oai:DiVA.org:umu-152417DiVA, id: diva2:1253529
Tilgjengelig fra: 2018-10-05 Laget: 2018-10-05 Sist oppdatert: 2018-10-05bibliografisk kontrollert

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