Nitrogen Source Dependent Changes in Central Sugar Metabolism Maintain Cell Wall Assembly in Mitochondrial Complex I-Defective frostbite1 and Secondarily Affect Programmed Cell Death. Podgórska, A., Ostaszewska-Bugajska, M., Tarnowska, A., Burian, M., Borysiuk, K., Gardeström, P., & Szal, B. International Journal of Molecular Sciences, 19(8):2206, July, 2018. ![Nitrogen Source Dependent Changes in Central Sugar Metabolism Maintain Cell Wall Assembly in Mitochondrial Complex I-Defective frostbite1 and Secondarily Affect Programmed Cell Death [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex 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.
@article{podgorska_nitrogen_2018,
title = {Nitrogen {Source} {Dependent} {Changes} in {Central} {Sugar} {Metabolism} {Maintain} {Cell} {Wall} {Assembly} in {Mitochondrial} {Complex} {I}-{Defective} frostbite1 and {Secondarily} {Affect} {Programmed} {Cell} {Death}},
volume = {19},
issn = {1422-0067},
url = {http://www.mdpi.com/1422-0067/19/8/2206},
doi = {10.3390/ijms19082206},
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.},
language = {en},
number = {8},
urldate = {2021-06-07},
journal = {International Journal of Molecular Sciences},
author = {Podgórska, Anna and Ostaszewska-Bugajska, Monika and Tarnowska, Agata and Burian, Maria and Borysiuk, Klaudia and Gardeström, Per and Szal, Bożena},
month = jul,
year = {2018},
pages = {2206},
}
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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. 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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. 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