MYB28 and MYB29 transcription factors regulate iron homeostasis and iron-mobilizing coumarin biosynthesis in Arabidopsis thaliana
Abstract
Iron (Fe) deficiency is a major constraint for plant growth and triggers extensive physiological and transcriptional reprogramming to maintain Fe homeostasis. Here, we identify the glucosinolate-associated transcription factors MYB28 and MYB29 as previously unrecognized regulators of Arabidopsis thaliana adaptation to Fe deficiency. Across various growth systems, loss of MYB28 increased sensitivity to Fe deficiency, whereas the myb28myb29 double mutant displayed stronger chlorosis, reduced root growth and impaired biomass accumulation, indicating cooperative but unequal functions of these transcription factors. Despite their enhanced Fe-deficiency phenotype, double mutant plants accumulated higher Fe levels in roots and exhibited stronger induction of canonical Fe-deficiency responses, suggesting impaired Fe utilization or distribution rather than defective Fe uptake. RNA-seq revealed extensive transcriptional reprogramming under Fe deficiency, with pronounced deregulation of genes involved in Fe homeostasis, redox processes and growth, particularly in the double mutant. Among these, SCOPOLETIN 8-HYDROXYLASE (S8H) emerged as a major target gene of MYB28. The expression of S8H was almost abolished in myb28 and myb28myb29 mutants, whereas expression of other coumarin biosynthetic genes remained largely unaffected. Promoter activation assays demonstrated that MYB28 activates the S8H promoter, and metabolic analyses showed accumulation of scopolin together with reduced fraxin levels in the mutants, consistent with impaired S8H activity. Collectively, our results identify MYB28 as a key regulator linking specialized metabolism to Fe homeostasis through control of coumarin biosynthesis, thereby expanding the biological functions of MYB28 and MYB29 transcription factors.
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BibTeX
@misc{marinpena2026myb28,
title = {{MYB28 and MYB29 transcription factors regulate iron homeostasis and iron-mobilizing coumarin biosynthesis in Arabidopsis thaliana}},
author = {Agustin Javier Marin-Pena and Inmaculada Coleto and Jose Alberto Urbano-Gamez and Alice Rossille and Diego Tazueco and Sunshuke Watanabe and Daniela Salazar-Gutierrez and Antonio Santiago and Meng-Bo Tian and Hannetz Roschzttardtz and Joaquin Medina and Jose Tomas Matus and Christian Dubos and Daniel Marino},
howpublished = {HAL},
year = {2026},
month = sep,
doi = {10.64898/2026.09.09.750326},
url = {https://hal.inrae.fr/hal-05751494v1},
note = {CC BY 4.0},
}
RIS
TY - UNPB
TI - MYB28 and MYB29 transcription factors regulate iron homeostasis and iron-mobilizing coumarin biosynthesis in Arabidopsis thaliana
AU - Agustin Javier Marin-Pena
AU - Inmaculada Coleto
AU - Jose Alberto Urbano-Gamez
AU - Alice Rossille
AU - Diego Tazueco
AU - Sunshuke Watanabe
AU - Daniela Salazar-Gutierrez
AU - Antonio Santiago
AU - Meng-Bo Tian
AU - Hannetz Roschzttardtz
AU - Joaquin Medina
AU - Jose Tomas Matus
AU - Christian Dubos
AU - Daniel Marino
PY - 2026
DA - 2026/09/09
PB - HAL
DO - 10.64898/2026.09.09.750326
UR - https://hal.inrae.fr/hal-05751494v1
AB - Iron (Fe) deficiency is a major constraint for plant growth and triggers extensive physiological and transcriptional reprogramming to maintain Fe homeostasis. Here, we identify the glucosinolate-associated transcription factors MYB28 and MYB29 as previously unrecognized regulators of Arabidopsis thaliana adaptation to Fe deficiency. Across various growth systems, loss of MYB28 increased sensitivity to Fe deficiency, whereas the myb28myb29 double mutant displayed stronger chlorosis, reduced root growth and impaired biomass accumulation, indicating cooperative but unequal functions of these transcription factors. Despite their enhanced Fe-deficiency phenotype, double mutant plants accumulated higher Fe levels in roots and exhibited stronger induction of canonical Fe-deficiency responses, suggesting impaired Fe utilization or distribution rather than defective Fe uptake. RNA-seq revealed extensive transcriptional reprogramming under Fe deficiency, with pronounced deregulation of genes involved in Fe homeostasis, redox processes and growth, particularly in the double mutant. Among these, SCOPOLETIN 8-HYDROXYLASE (S8H) emerged as a major target gene of MYB28. The expression of S8H was almost abolished in myb28 and myb28myb29 mutants, whereas expression of other coumarin biosynthetic genes remained largely unaffected. Promoter activation assays demonstrated that MYB28 activates the S8H promoter, and metabolic analyses showed accumulation of scopolin together with reduced fraxin levels in the mutants, consistent with impaired S8H activity. Collectively, our results identify MYB28 as a key regulator linking specialized metabolism to Fe homeostasis through control of coumarin biosynthesis, thereby expanding the biological functions of MYB28 and MYB29 transcription factors.
ER -