Abstract：
:By functioning as an enzyme cofactor, hemoglobin component, and gene regulator, heme is vital for life. One mode of heme-regulated transcription involves amplifying the activity of GATA-1, a key determinant of erythrocyte differentiation. To discover biological consequences of the metal cofactor-transcription factor mechanism, we merged GATA-1/heme-regulated sectors of the proteome and transcriptome. This multi-omic analysis revealed a GATA-1/heme circuit involving hemoglobin subunits, ubiquitination components, and proteins not implicated in erythrocyte biology, including the zinc exporter Slc30a1. Though GATA-1 induced expression of Slc30a1 and the zinc importer Slc39a8, Slc39a8 dominantly increased intracellular zinc, which conferred erythroblast survival. Subsequently, a zinc transporter switch, involving decreased importer and sustained exporter expression, reduced intracellular zinc during terminal differentiation. Downregulating Slc30a1 increased intracellular zinc and, strikingly, accelerated differentiation. This analysis established a conserved paradigm in which a GATA-1/heme circuit controls trace metal transport machinery and trace metal levels as a mechanism governing cellular differentiation.
journal_name
Dev Celljournal_title
Developmental cellauthors
Tanimura N,Liao R,Wilson GM,Dent MR,Cao M,Burstyn JN,Hematti P,Liu X,Zhang Y,Zheng Y,Keles S,Xu J,Coon JJ,Bresnick EHdoi
10.1016/j.devcel.2018.07.022subject
Has Abstractpub_date
2018-09-10 00:00:00pages
581-594.e4issue
5eissn
1534-5807issn
1878-1551pii
S1534-5807(18)30607-5journal_volume
46pub_type
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