Posttranslational Regulation of the Iron Deficiency Basic Helix-Loop-Helix Transcription Factor FIT Is Affected by Iron and Nitric Oxide      

Abstract

Understanding iron (Fe) sensing and regulation is important for targeting key genes for important nutritional traits like Fe content. The basic helix-loop-helix transcription factor FIT (for FER-LIKE FE DEFICIENCY-INDUCED TRANSCRIPTION FACTOR) controls Fe acquisition genes in dicot roots. Posttranscriptional regulation of transcription factors allows rapid adaptation to cellular changes and was also described for FIT. However, the mechanisms behind this regulation of FIT were for a long time not known. Here, we studied the posttranscriptional control mechanisms of FIT in Arabidopsis (Arabidopsis thaliana) and identified nitric oxide as a stabilizing stimulus for FIT protein abundance. Using cycloheximide, we confirmed that the level of FIT protein was regulated by way of protein turnover in wild-type and hemagglutinin-FIT plants. Upon cycloheximide treatment, FIT activity was hardly compromised, since Fe deficiency genes like IRON-REGULATED TRANS-PORTER1 and FERRIC REDUCTASE OXIDASE2 were still inducible by Fe deficiency. A small pool of "active" FIT was sufficient for the induction of Fe deficiency downstream responses. Nitric oxide inhibitors caused a decrease of FIT protein abundance and, in the wild type, also a decrease in FIT activity. This decrease of FIT protein levels was reversed by the proteasomal inhibitor MG132, suggesting that in the presence of nitric oxide FIT protein was less likely to be a target of proteasomal degradation. Independent of FIT transcription, FIT protein stability and FIT protein activity, therefore, were targets of control mechanisms in response to Fe and nitric oxide. We summarize our results in a model that explains the different steps of FIT regulation integrating the plant signals that control FIT.

Similarities and Differences in the Acquisition of Fe and P by Dicot Plants

“…In addition to ethylene, other hormones and signaling substances, such as auxin and nitric oxide (NO), have been involved in the up-regulation of Fe and P acquisition genes [3,4,29,68,[75][76][77][78][79][80][81]. In both deficiencies, the activating effect of auxin, ethylene and NO depend on the Fe or P status of the plants [68,69,75,76], which suggests the existence of additional Fe-and P-related signals acting in conjunction with ethylene, auxin and NO [82].…”

Relationship between tree nutritional status and apple quality

“…NR and NiR), Fe deficiency could alter the cytosolic concentration leading to a restriction of its uptake mechanisms (Nikolic et al 2007). From microarray data some information is available concerning the Fedeficient-dependent expression of genes related to (Meiser et al 2011). …”

ZINC FINGER OF ARABIDOPSIS THALIANA12 (ZAT12) Interacts with FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR (FIT) Linking Iron Deficiency and Oxidative Stress Responses

“…FIT is also a central hub for the input of multiple signaling pathways. FIT action is upregulated by Fe deficiency (Colangelo and Guerinot, 2004;Jakoby et al, 2004) in response to ethylene (García et al, 2010(García et al, , 2011Lingam et al, 2011) and nitric oxide (NO; Chen et al, 2010;Meiser et al, 2011) and is down-regulated by cytokinins (Séguéla et al, 2008) and jasmonic acid (Maurer et al, 2011; for review, see Brumbarova et al, 2015). The cross-link between FIT and diverse signaling pathways allows the plants to modulate Fe nutrition in adaptation to changing growth conditions.…”

“…The FIT gene transcription is elicited by Fe deficiency as part of an autoregulatory loop requiring the FIT protein itself (Wang et al, 2007) and is also modulated by ethylene and NO signaling (García et al, 2010;Lingam et al, 2011;Meiser et al, 2011). Furthermore, ethylene and NO control the levels and stability of the FIT protein Meiser et al, 2011).…”