AtFC1 Overexpression Confers Plant Tolerance to Cadmium Toxicity

Non-essential trace metals such as cadmium (Cd) are toxic to plants. While some plants have developed ways to deal with absorbed Cd, the regulatory mechanisms behind the Cd tolerance are not fully understood. Ferrochelatase-1 (FC1), the terminal enzyme of heme biosynthesis, have been shown to be involved in several physiological processes. However, its function associated with plant abiotic stress response is poorly understood. Jun Song and Sheng Jun Feng from Nanjing Agricultural University aimed to learn more of FC1 from Arabidopsis.

Analysis showed that AtFC1 is activated by Cd exposure. AtFC1 overexpressing lines accumulated more Cd than wild types, and exhibited enhanced plant tolerance to Cd stress. The overexpressing lines also exhibited improved primary root elongation, biomass and chlorophyll contents. In contrast, the AtFC1 loss-of-function mutants showed sensitivity to Cd stress. Exogenous application of heme, the product of AtFC1, partially rescued the Cd-induced toxic phenotype of loss-of-function mutants. Further analysis showed that disfunction of AtFC1 led to 913 genes specifically upregulated and 522 genes downregulated in loss-of-function mutants exposed to Cd. Some of these genes are involved in metal transport, Cd-induced oxidative stress response, and detoxification.

These results indicate that AtFC1 acts as a positive regulator of plant tolerance to Cd stress. This study will serve as reference for studies on the role of FC1 in mediating plant response to Cd stress.

For more information on this study, read the article in BMC Plant Biology.