MPK3-mediated phosphorylation inactivates MYB4 to promote FIT-dependent iron acquisition
TL;DR
This work unveils the MPK3-MYB4-FIT signaling module as a previously unrecognized regulatory module that contributes to the dynamic control of Fe homeostasis in Arabidopsis.
Abstract
Iron (Fe) is an essential micronutrient for plant growth, and its homeostasis is critically regulated by the transcription factor FIT in response to deficiency. Here, we identify the R2R3-MYB transcription factor MYB4 as a previously unknown negative regulator of Fe acquisition. MYB4 directly interacts with FIT, competing with bHLH38/39 to prevent the formation of transcriptionally active heterodimers, thereby repressing the expression of the key Fe-uptake genes IRT1 and FRO2. We establish that the mitogen-activated protein kinase MPK3 acts upstream in this pathway. Under Fe-deficient conditions, MPK3 is activated and directly phosphorylates MYB4 at Serine 4, promoting its proteasome-dependent destabilization. This post-translational switch releases FIT to dimerize with bHLH partners, activating Fe uptake. Our work unveils the MPK3-MYB4-FIT signaling module as a previously unrecognized regulatory module that contributes to the dynamic control of Fe homeostasis in Arabidopsis. Iron (Fe) deficiency activates MPK3-mediated phosphorylation of MYB4, triggering MYB4 degradation and releasing FIT-bHLH38/39 complex activity. This phospho-switch mechanism controls Fe uptake gene expression and maintains Fe homeostasis in Arabidopsis. MYB4 inhibits FIT-bHLH38/39 complex formation and suppresses Fe uptake gene expression during Fe sufficiency. MPK3 phosphorylates MYB4 to promote its ubiquitin-dependent degradation during Fe deficiency. Loss of MYB4 promotes Fe acquisition and Fe deficiency tolerance through activation of the FIT pathway. The MPK3-MYB4-FIT module provides post-translational control of plant Fe homeostasis. MYB4 inhibits FIT-bHLH38/39 complex formation and suppresses Fe uptake gene expression during Fe sufficiency. MPK3 phosphorylates MYB4 to promote its ubiquitin-dependent degradation during Fe deficiency. Loss of MYB4 promotes Fe acquisition and Fe deficiency tolerance through activation of the FIT pathway. The MPK3-MYB4-FIT module provides post-translational control of plant Fe homeostasis. Iron (Fe) deficiency activates MPK3-mediated phosphorylation of MYB4, triggering MYB4 degradation and releasing FIT-bHLH38/39 complex activity. This phospho-switch mechanism controls Fe uptake gene expression and maintains Fe homeostasis in Arabidopsis.