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.

[bmcplantbiol.biomedcentral.com]