by Sanjay Mishra
Iron and sulfur are essential minerals critically required for biological functions. The body maintains iron levels through iron homeostasis. Deficiency in iron uptake can cause anemia and excess iron accumulation can lead to organ failure. Similarly, sulfur is incorporated into biological compounds through an ancient pathway called sulfur assimilation.
Now in a study published in the Proceedings of the National Academy of Sciences, John York, PhD, and colleagues report an unanticipated link between the sulfur assimilation pathway and iron homeostasis.
Bpnt1 is a key regulator of the sulfur assimilation pathway. Deletion of Bpnt1 in mice led to toxic accumulation of its substrate, PAP, which in turn caused iron-deficiency anemia. When a genetic mutation that reduced PAP synthesis was introduced into the mice, PAP accumulation fell and anemia was avoided.
The study thus defines a genetic basis for iron-deficiency anemia. It is reasonable to add Bpnt1 as a possible gene to sequence in patients with the disease, the researchers concluded.
This research was supported by funds from the Vanderbilt Medical Scientist Training Program (GM007347), Howard Hughes Medical Institute and Vanderbilt University.
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