Mitochondrial iron transport via MFRN1 is required for erythroid cell cycle progression.

ABSTRACT:

Abstract

Iron metabolism drives key erythropoietic processes, including hemoglobinization, survival, and proliferation. Here, we developed in vivo methods to interrogate how iron regulates erythropoiesis and report that mitochondrial iron transport via mitoferrin-1 (MFRN1) is essential for erythroid cell cycle progression. mfrn1 embryos had severely decreased erythroid cell number caused by cell cycle arrest at G2/M. They had enlarged nuclei, suggesting a mitotic defect. Iron supplementation rescued the cell cycle defect, implicating mitochondrial iron deficiency as its cause. In contrast, fpn1 mutants, anemic from systemic iron deficiency, had less severe decreases in erythroid mitochondrial iron than mfrn1 mutants and no proliferative defects. Single-cell RNA sequencing and fluor

SUBMITTER: Perfetto M 

PROVIDER: S-EPMC12657292 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature