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Summary    The key basic helix–loop–helix ( bHLH ) transcription factor in iron (Fe) uptake,  FER ‐ LIKE IRON DEFICIENCY ‐ INDUCED TRANSCRIPTION FACTOR  ( FIT ), is controlled by multiple signaling pathways, important to adjust Fe acquisition to growth and environmental constraints.  FIT  protein exists in active and inactive protein pools, and phosphorylation of serine Ser272 in the C‐terminus, a regulatory domain of  FIT , provides a trigger for  FIT  activation.  Here, we use phospho‐mutant activity assays and study phospho‐mimicking and phospho‐dead mutations of three additional predicted phosphorylation sites, namely at Ser221 and at tyrosines Tyr238 and Tyr278, besides Ser 272.  Phospho‐mutations at these sites affect  FIT  activities in yeast, plant, and mammalian cells. The diverse array of cellular phenotypes is seen at the level of cellular localization, nuclear mobility, homodimerization, and dimerization with the  FIT ‐activating partner  bHLH 039, promoter transactivation, and protein stability. Phospho‐mimicking Tyr mutations of  FIT  disturb  fit  mutant plant complementation.  Taken together, we provide evidence that  FIT  is activated through Ser and deactivated through Tyr site phosphorylation. We therefore propose that  FIT  activity is regulated by alternative phosphorylation pathways.

new phytologist

Phospho‐mutant activity assays provide evidence for alternative phospho‐regulation pathways of the transcription factor  FER‐LIKE IRON DEFICIENCY‐INDUCED TRANSCRIPTION FACTOR