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. 2016 Jan 5;6:1185. doi: 10.3389/fpls.2015.01185

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Copyright © 2016 Vigani and Briat.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematized model of the possible role of mitochondria in the regulation of nutrient-responsive genes. As Fe and S are essential elements for Fe–S cluster-containing proteins, deficiencies of such nutrients trigger mitochondrial dysfunctions mainly at the respiratory chain level. Through the comparison of different data sets (mitochondrial dysfunctions vs. Fe- and/or S-responsive genes), nutrient-responsive genes have been identified as potential candidates of hypothetical retrograde signaling pathways (PYE, BTS, FRO3; OPT3, SAM1 for Fe homeostasis and SULTR1;2 SULTR3;4, SULTR4;2, LSU1, BGLU28, SDI1 for S homeostasis). Mitochondrial impairments occur in long term of Fe and S starvations; therefore, such retrograde signaling would occur in a second phase of the regulation of nuclear gene expression, whereas the first phase (gray arrows) involved a more direct nutrient-sensing mechanisms.