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Nature study reveals loss of essential blood cell gene leads to anemia
Date:11/13/2012

f ferrochelatase, was brought on board. Collaborative work between the Paw and Dailey laboratories uncovered a broader mechanistic role for Atpif1 in regulating the enzymatic activity of ferrochelatase.

"We believe that the two iron-two sulfur (2Fe- 2S) cluster of ferrochelatase allows it to sense certain metabolic fluxes in the cell and respond to those fluxes in an appropriate way," said Dailey, who is a professor of microbiology and director of the UGA Biomedical and Health Sciences Institute. "When Atpf1 is deficient, there is a change in the mitochondrial pH/redox potential. This change is sensed by the cluster, and ferrochelatase activity is turned down, which results in diminished heme synthesis."

The researchers also were able to produce data on the human version of Atpif1, noting its functional importance for normal red blood cell differentiation as well as how a deficiency may contribute to human diseasessuch as congenital anemias and disorders related to dysfunctional mitochondria, the organelles that power the cell.

Overall, Dailey believes the study's results will impact the field of red blood cell development significantly with the establishment of the ferrochelatase [2Fe-2S] cluster as a new regulatory component in heme synthesis. New areas of investigation will open, he said, and the molecular basis of currently undefined red blood cell-based syndromes and diseases may be revealed.


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Contact: Harry Dailey
hdailey@uga.edu
706-542-5922
University of Georgia
Source:Eurekalert

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