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Zhang, H. M.

Publications and source records attributed to Zhang, H. M..

2 recordsLinked to original sources

FER-LIKE FE DEFICIENCY-INDUCED TRANSCRIPTION FACTOR (OsFIT) interacts with OsIRO2 to regulate iron homeostasis

There are two Fe-uptake strategies for maintaining Fe homeostasis in plants. As a special graminaceous plant, rice applies both strategies. However, it remains unclear how these two strategies are regulated in rice. IRON-RELATED BHLH TRANSCRIPTION FACTOR 2 (OsIRO2) is critical for regulating Fe uptake in rice. In this study, we identified an interacting partner of OsIRO2, Oryza sativa FER-LIKE FE DEFICIENCY-INDUCED TRANSCRIPTION FACTOR (OsFIT), which encodes a bHLH transcription factor. The OsIRO2 protein is localized in the cytoplasm and nucleus, but OsFIT facilitates the accumulation of OsIRO2 in the nucleus. Loss-of-function mutations to OsFIT result in decreased Fe accumulation, severe Fe-deficiency symptoms, and disrupted expression of Fe-uptake genes. In contrast, OsFIT overexpression promotes Fe accumulation and the expression of Fe-uptake genes. Genetic analyses indicated that OsFIT and OsIRO2 function in the same genetic node. Further analysis suggested that OsFIT and OsIRO2 form a functional transcription activation complex to initiate the expression of Fe-uptake genes. Our findings provide a mechanism understanding of how rice maintains Fe homeostasis. One-sentence summaryOsFIT interacts with and facilitates the accumulation of OsIRO2 in the nucleus where the OsFIT-OsIRO2 transcription complex initiates the transcription of Fe deficiency responsive genes.

plant biology↗

Bisphenol A promotes stress granule assembly and modulates the integrated stress response

Bisphenol-A (BPA) is a ubiquitous precursor of polycarbonate plastics that is found in the blood and serum of >92% of Americans. While BPA has been well documented to act as a weak estrogen receptor (ER) agonist, its effects on cellular stress are unclear. Here, we demonstrate that high-dose BPA causes stress granules (SGs) in human cells. A common estrogen derivative, {beta}-estradiol, does not trigger SGs, indicating the mechanism of SG induction is not via the ER pathway. We also tested other structurally related environmental contaminants including the common BPA substitutes BPS and BPF, the industrial chemical 4-nonylphenol (4-NP) and structurally related compounds 4-EP and 4-VP, and the pesticide 2,4-dichlorophenoxyacetic acid (2,4-D). The variable results from these related compounds suggest that structural homology is not a reliable predictor of the capacity of a compound to cause SGs. Also, we demonstrate that BPA acts primarily through the PERK pathway to generate canonical SGs. Finally, we show that chronic exposure to a low physiologically relevant dose of BPA disrupts SG assembly by inhibiting SGs upon additional acute stress. Our work identifies additional effects of BPA beyond endocrine disruption that may have consequences for human health.

cell biology↗