Sox17 is turned on in blood-forming stem cells in fetal mice but not in adults.

A University of Michigan research team have found a gene, Sox17, required for the maintenance of blood-forming stem cells in fetal mice but not in adult mice. This provides insight into the mechanisms that distinguish fetal blood-forming stem cells from their adult counterparts.

“One of the next questions in our crosshairs is whether Sox17 gets inappropriately activated in certain childhood leukemias—and that’s an idea that nobody had in their mind before this work,” says Sean Morrison, Ph.D., team leader and associate professor of cell and developmental biology.

The investigators looked for genes required to maintain hematopoietic stem cells in fetal mice but not in adult mice. They found that Sox17 was turned on in fetal and neonatal hematopoietic stem cells but not adult hematopoietic stem cells.

To test whether Sox17 was functionally important for fetal and neonatal blood-forming stem cells, the scientists deleted the gene in laboratory mice. This led to the loss of fetal and neonatal but not adult hematopoietic stem cells.

In follow-up experiments, mice were irradiated to destroy their blood-forming stem cells. Then replacement fetal or neonatal blood-forming cells were transplanted into the mice, some containing the Sox17 gene and others lacking it. The mice that received Sox17-bearing cells were able to regenerate their blood systems. Those that received cells lacking the gene could not.

The results will be published online July 26 in Cell.

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