AUTHOR=Khan Muhammad Sayyar , Lu Qiao , Cui Man , Rajab Hala , Wu Huilan , Chai Tuanyao , Ling Hong-Qing 

TITLE=Crosstalk Between Iron and Sulfur Homeostasis Networks in Arabidopsis

JOURNAL=Frontiers in Plant Science

VOLUME=13

YEAR=2022

URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2022.878418

DOI=10.3389/fpls.2022.878418

ISSN=1664-462X

ABSTRACT=<p>The widespread deficiency of iron (Fe) and sulfur (S) is becoming a global concern. The underlying mechanisms regulating Fe and S sensing and signaling have not been well understood. We investigated the crosstalk between Fe and S using mutants impaired in Fe homeostasis, sulfate assimilation, and glutathione (GSH) biosynthesis. We showed that chlorosis symptoms induced by Fe deficiency were not directly related to the endogenous GSH levels. We found dynamic crosstalk between Fe and S networks and more interestingly observed that the upregulated expression of <italic>IRT1</italic> and <italic>FRO2</italic> under S deficiency in Col-0 was missing in the <italic>cad2-1</italic> mutant background, which suggests that under S deficiency, the expression of <italic>IRT1</italic> and <italic>FRO2</italic> was directly or indirectly dependent on GSH. Interestingly, the bottleneck in sulfite reduction led to a constitutively higher <italic>IRT1</italic> expression in the <italic>sir1-1</italic> mutant. While the high-affinity sulfate transporter (<italic>Sultr1;2</italic>) was upregulated under Fe deficiency in the roots, the low-affinity sulfate transporters (<italic>Sultr2;1,</italic> and <italic>Sultr2;2</italic>) were down-regulated in the shoots of Col-0 seedlings. Moreover, the expression analysis of some of the key players in the Fe–S cluster assembly revealed that the expression of the so-called Fe donor in mitochondria (<italic>AtFH</italic>) and S mobilizer of group II cysteine desulfurase in plastids (<italic>AtNFS2</italic>) were upregulated under Fe deficiency in Col-0. Our qPCR data and ChIP-qPCR experiments suggested that the expression of <italic>AtFH</italic> is likely under the transcriptional regulation of the central transcription factor <italic>FIT.</italic></p>