AtHO1 (HY1) encodes heme oxygenase-1 in Arabidopsis, catalyzing cleavage of heme to biliverdin with the release of iron and carbon monoxide (CO). Our previous study showed that CO as an endogenous component is able to improve plant adaptation to iron deficiency. Here, we performed a genetic study to identify further the putative role of AtHO1 in the iron deficiency response. Iron deficiency induced AtHO1 expression at the transcriptional and translational levels. Evidence has been provided that overexpression of AtHO1 could confer plant tolerance to iron deficiency by improving expression of AtFIT, AtFRO2 and AtIRT1, the activity of ferric-chelate reductase (FCR) and iron accumulation. In contrast, RNA interference with AtHO1 expression in 35S::AntiHO1 plants and the AtHO1 loss-of-function (hy1 mutant) resulted in adverse phenotypes. In 35S::AtHO1 transgenic lines, a higher level of CO and water-soluble iron, and a lower level of heme were identified, suggesting that AtHO1-regulated iron homeostasis was possibly through the catabolism of heme to produce CO and free iron. Because nitric oxide (NO) is known to regulate iron homeostasis in plants, the connection between AtHO1 expression and NO action was examined. AtHO1-overexpressing plants generated more NO, whereas knock-down of AtHO1 expression reduced the level of NO in plants. The NO scavenger cPTIO [2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethylini dazoline-1-oxyl-3-oxide] caused a decrease in AtHO1-induced FCR activity. Under both iron-sufficient and -deficient conditions, administration of the NO donor sodium nitroprusside induced FCR activity in the hy1 plants. These results suggest that AtHO1 is involved in iron homeostasis in an NO-dependent manner.
Keywords: Arabidopsis; Carbon monoxide; Heme oxygenase-1; Homeostasis; Iron deficiency.