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Ferrochelatase-1 as a terminal enzyme of heme biosynthesis regulates many essential metabolic and physiological processes. Whether FC1 is involved in plant response to salt stress has not been described. This study shows that Arabidopsis overexpressing  AtFC1  displays resistance to high salinity, whereas a T-DNA insertion knock-down mutant  fc1  was more sensitive to salt stress than wild-type plants.  AtFC1  conferred plant salt resistance by reducing Na +  concentration, enhancing K +  accumulation and preventing lysis of the cell membrane. Such observations were associated with the upregulation of  SOS1 , which encodes a plasma membrane Na + /H +  antiporter.  AtFC1  overexpression led to a reduced expression of several well known salt stress-responsive genes such as  NHX1  and  AVP1 , suggesting that  AtFC1 -regulated low concentration of Na +  in plants might not be through the mechanism for Na +  sequestration. To investigate the mechanism leading to the role of  AtFC1  in mediating salt stress response in plants, a transcriptome of  fc1  mutant plants under salt stress was profiled. Our data show that mutation of  AtFC1  led to 490 specific genes up-regulated and 380 specific genes down-regulated in  fc1  mutants under salt stress. Some of the genes are involved in salt-induced oxidative stress response, monovalent cation-proton (Na + /H + ) exchange, and Na +  detoxification.

Salt stress-induced FERROCHELATASE 1 improves resistance to salt stress by limiting sodium accumulation in Arabidopsis thaliana