Abstract
Global population increases and climate change underscore the need for better comprehension of how plants acquire and process nutrients such as iron. Using cell type-specific transcriptional profiling, we identified a pericycle-specific iron deficiency response and a bHLH transcription factor, POPEYE (PYE), that may play an important role in this response. Functional analysis of PYE suggests that it positively regulates growth and development under iron-deficient conditions. Chromatin immunoprecipitation-on-chip analysis and transcriptional profiling reveal that PYE helps maintain iron homeostasis by regulating the expression of known iron homeostasis genes and other genes involved in transcription, development, and stress response. PYE interacts with PYE homologs, including IAA-Leu Resistant3 (ILR3), another bHLH transcription factor that is involved in metal ion homeostasis. Moreover, ILR3 interacts with a third protein, BRUTUS (BTS), a putative E3 ligase protein, with metal ion binding and DNA binding domains, which negatively regulates the response to iron deficiency. PYE and BTS expression is also tightly coregulated. We propose that interactions among PYE, PYE homologs, and BTS are important for maintaining iron homeostasis under low iron conditions.
Highlights
Iron is an essential nutrient for both plants and animals
We selected and screened 38 T-DNA insertion mutants of putative transcription factors whose expression is affected during the iron deficiency time course
Using cell type–specific transcriptional profiling, we found that the stele, which includes the pericycle, is the most responsive cell type within the root (Dinneny et al, 2008)
Summary
Iron is an essential nutrient for both plants and animals. In most human populations, nutritional iron is obtained predominantly from plants. Plants have evolved different mechanisms to solubilize and absorb iron from soil (Schmidt, 1999; Walker and Connolly, 2008; Palmer and Guerinot, 2009). Nongraminaceous plants such as Arabidopsis thaliana respond to iron deficiency with increased expression of the bHLH transcription factor FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR (FIT) (Bauer et al, 2007) whose protein forms heterodimers with bHLH protein bHLH38 or bHLH39 (Yuan et al, 2008). FIT positively regulates expression of FRO2, which encodes an epidermal iron reductase that reduces ferric iron in response to iron deficiency (Robinson et al, 1999). FIT positively regulates the accumulation of IRT1 protein, which transports reduced Fe2+ into the symplast
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