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Key message
ILR3 and PYE function in a regulatory network that modulates GLS accumulation under iron deficiency.
The molecular processes involved in the cross talk between iron (Fe) homeostasis and other metabolic processes in plants are poorly understood. In
Arabidopsis thaliana
the transcription factor IAA-LEUCINE RESISTANT3 (ILR3) regulates iron deficiency response, aliphatic glucosinolate (GLS) biosynthesis and pathogen response. ILR3 is also known to interact with its homolog, POPEYE (PYE), which also plays a role in Fe response. However, little is known about how ILR3 regulates such diverse processes, particularly, via its interaction with PYE. Since GLS are produced as part of a defense mechanism against wounding pathogens, we examined
pILR3::β-GLUCURONIDASE
expression and found that Fe deficiency enhances the wound-induced expression of ILR3 in roots and that ILR3 is induced in response to the wounding pathogen, sugarbeet root cyst nematode (
Heterodera schachtii
). We also examined the expression pattern of genes involved in Fe homeostasis and aliphatic GLS biosynthesis in
pye-1, ilr3-2
and
pye-1xilr3-2 (pxi)
mutants and found that ILR3 and PYE differentially regulate the expression of genes involved these processes under Fe deficiency. We measured GLS levels and sugarbeet root cyst nematode infection rates under varying Fe conditions, and found that long-chain GLS levels are elevated in
ilr3-2
and
pxi
mutants. This increase in long-chain GLS accumulation is correlated with elevated nematode resistance in
ilr3-2
and
pxi
mutants in the absence of Fe. Our findings suggest that ILR3 and PYE function in a regulatory network that controls wounding pathogen response in plant roots by modulating GLS accumulation under iron deficiency.