Abstract
The switch from Hb F to A which occurs during ontogeny in primates is incomplete in the adult. In addition, Hb F may reappear during erythroid stress. Colonies derived in vitro from erythroid progenitors also produce both Hbs F and A. At each stage of normal ontogeny, the relation between the proportion of F synthesized in the colonies derived from progenitors in vitro and in the reticulocytes or erythroblasts (precursors) which developed in vivo is not immediately apparent. There are several possible models to explain the phenomenon of the ontogenic switch. A cellular model is presented.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 111-116 |
| Number of pages | 6 |
| Journal | Birth Defects: Original Article Series |
| Volume | 18 |
| Issue number | 7 |
| State | Published - 1982 |
| Externally published | Yes |
ASJC Scopus subject areas
- Developmental Biology
- Genetics(clinical)