Figures
A fungal ABC transporter FgAtm1 regulates iron homeostasis via the transcription factor cascade FgAreA-HapX
As a mitochondrial ABC transporter in Fusarium graminearum, FgAtm1 regulates the activity of cytosolic Fe-S proteins via transporting GSH-linked [2Fe-2S] clusters from mitochondria into cytoplasm. The lack of FgAtm1 reduces the activity of cytosolic Fe-S proteins nitrite reductase and xanthine dehydrogenase, which causes high expression of iron regulator FgHapX via activating the transcription factor FgAreA. FgHapX represses transcription of the genes for iron-consuming proteins, but activates the genes for iron-acquisition proteins. The image indicates that the growth of ΔFgAtm1 is accelerated by feeding with each of the final catalytic products of cytosolic Fe-S proteins. Wang et al.
Image Credit: Z Wang, Y Yin, and Z Ma (2019)
Citation: (2019) PLoS Pathogens Issue Image | Vol. 15(9) September 2019. PLoS Pathog 15(9): ev15.i09. https://doi.org/10.1371/image.ppat.v15.i09
Published: September 27, 2019
Copyright: © 2019 . This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
As a mitochondrial ABC transporter in Fusarium graminearum, FgAtm1 regulates the activity of cytosolic Fe-S proteins via transporting GSH-linked [2Fe-2S] clusters from mitochondria into cytoplasm. The lack of FgAtm1 reduces the activity of cytosolic Fe-S proteins nitrite reductase and xanthine dehydrogenase, which causes high expression of iron regulator FgHapX via activating the transcription factor FgAreA. FgHapX represses transcription of the genes for iron-consuming proteins, but activates the genes for iron-acquisition proteins. The image indicates that the growth of ΔFgAtm1 is accelerated by feeding with each of the final catalytic products of cytosolic Fe-S proteins. Wang et al.
Image Credit: Z Wang, Y Yin, and Z Ma (2019)