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

Regulation of ZAT12 protein stability: The role of hydrogen peroxide

“…Under excess of free cellular Fe, ROS is generated as a result of the Fenton reaction, 12 while under Fe deficiency, a consistently elevated ROS production, probably as a signaling intermediate, was shown to be dependent on FIT activity. 8 Consistent with this, FIT was revealed as a target for negative regulation by ZAT12 through direct ZAT12-FIT protein interaction and inhibition of FIT gene expression. It was suggested that ZAT12 can sequester FIT protein molecules, preventing them from activating Fe acquisition.…”

“…1A). 8 We present here a model aiming to explain these findings and predict the types of potential regulators involved in ZAT12 degradation (Fig. 1B-E).…”

“…11,[13][14][15] It was found that ZAT12 undergoes proteasome-dependent degradation, which occurs also in the presence of elevated H 2 O 2 levels. 8 Deletion analysis showed that the EAR motif, which ZAT12 employs for the interaction with FIT, is essential for this proteasome targeting. ZAT12 proteins without EAR motif are degraded by different pathways, depending on the presence or absence of H 2 O 2 (summarized in Fig.…”

“…It was suggested that ZAT12 can sequester FIT protein molecules, preventing them from activating Fe acquisition. 8 Of special interest is to understand the role of ROS, in the form of hydrogen peroxide (H 2 O 2 ), in the regulation of ZAT12 stability in the epidermis of the early differentiation zone of the root, which is the essential zone for Fe acquisition under deficient Fe supply. 11,[13][14][15] It was found that ZAT12 undergoes proteasome-dependent degradation, which occurs also in the presence of elevated H 2 O 2 levels.…”

“…4,6,7 Recently, we showed that ZAT12 links ROS signaling and iron (Fe) acquisition, by directly interacting with the bHLH transcription factor FIT. 8 FIT acts as a central transcriptional regulator of the Fe deficiency-induced strategy for Fe acquisition from the soil. This strategy is based on 3 steps: (i) soil acidification, mainly conferred by the H C -ATPase AHA2, (ii) Fe (III) reduction by the FERRIC REDUCTASE-OXIDASE 2 (FRO2), and (iii) subsequent Fe(II) uptake by the IRON-REGULATED TRANSPORTER 1 (IRT1), whereby FIT upregulates AHA2, FRO2 and IRT1 upon Fe starvation.…”