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 .
Auxin and brassinosteroids (BRs) are two major growth-promoting phytohormones that shape hypocotyl elongation; however, the cross-talk between auxin and BR in this process is not fully understood. In this study, we found that auxin-induced hypocotyl elongation is dependent on brassinazole-resistant 1 (BZR1), a core BR signaling component. Auxin promotes BZR1 nuclear accumulation in hypocotyl cells, a process dependent on mitogen-activated protein kinase 3 (MPK3) and MPK6, which are both activated by auxin and whose encoding genes are highly expressed in hypocotyls. We determined that MPK3/MPK6 phosphorylate and reduce the protein stability of general regulatory factor 4 (GRF4), a member of the 14-3-3 family of proteins that retain BZR1 in the cytoplasm. In summary, this study reveals the molecular mechanism by which auxin promotes hypocotyl elongation by enhancing BZR1 nuclear accumulation via MPK3/MPK6-regulated GRF4 protein stability.
危险品化学品经营许可证（带存储）