Abstract:
:Sulfur assimilation is an evolutionarily conserved pathway that plays an essential role in cellular and metabolic processes, including sulfation, amino acid biosynthesis, and organismal development. We report that loss of a key enzymatic component of the pathway, bisphosphate 3'-nucleotidase (Bpnt1), in mice, both whole animal and intestine-specific, leads to iron-deficiency anemia. Analysis of mutant enterocytes demonstrates that modulation of their substrate 3'-phosphoadenosine 5'-phosphate (PAP) influences levels of key iron homeostasis factors involved in dietary iron reduction, import and transport, that in part mimic those reported for the loss of hypoxic-induced transcription factor, HIF-2α. Our studies define a genetic basis for iron-deficiency anemia, a molecular approach for rescuing loss of nucleotidase function, and an unanticipated link between nucleotide hydrolysis in the sulfur assimilation pathway and iron homeostasis.
journal_name
Proc Natl Acad Sci U S Aauthors
Hudson BH,Hale AT,Irving RP,Li S,York JDdoi
10.1073/pnas.1715302115subject
Has Abstractpub_date
2018-03-20 00:00:00pages
3000-3005issue
12eissn
0027-8424issn
1091-6490pii
1715302115journal_volume
115pub_type
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