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Evidence for a clonal model for hemoglobin switching.

B P Alter, R S Weinberg, J D Goldberg

    Progress in Clinical and Biological Research
    |January 1, 1983
    PubMed
    Summary
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    The switch from fetal to adult hemoglobin involves distinct progenitor cells. Studies in rhesus monkeys and human newborns reveal different progenitor cell populations driving this hemoglobin switch.

    Area of Science:

    • Hematology
    • Developmental Biology
    • Genetics

    Background:

    • The transition from fetal hemoglobin (Hb F) to adult hemoglobin (Hb A) is a critical developmental process.
    • This switch is thought to involve changes in erythroid progenitor cells and their hemoglobin expression programs.

    Purpose of the Study:

    • To investigate the role of distinct erythroid progenitor cell populations in the fetal-to-adult hemoglobin switch.
    • To analyze globin synthesis in single colonies derived from BFU-E (burst-forming unit-erythroid) in human newborns and rhesus fetuses.

    Main Methods:

    • Culturing BFU-E from human newborns and rhesus fetuses.
    • Analyzing globin synthesis (beta and gamma) in single erythroid colonies.
    • Differentiating between fetal and adult progenitor populations based on beta-globin synthesis levels.

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    Main Results:

    • Rhesus fetal colonies showed a bimodal distribution of beta-globin synthesis, suggesting multiple progenitor classes.
    • Human newborn cultures revealed late-emerging colonies from immature progenitors with altered globin synthesis correlations.
    • Fetal progenitors exhibit high Hb F and G gamma with correlated synthesis, while adult-like progenitors show lower, uncorrelated levels.

    Conclusions:

    • The hemoglobin switch is supported by a clonal model involving distinct progenitor cell populations.
    • Fetal progenitors persist in newborns, alongside the emergence of adult-like progenitors.
    • Understanding these progenitor dynamics is key to comprehending hemoglobin ontogeny.