Comparison of the Pf4-Cre and Gp1ba-Cre mice
| Pf4-Cre mice . | Gp1ba-Cre mice . |
|---|---|
| Pluses | |
| • Long prior experience and published literature with this system | • The Cre insert is in the native Gp1ba gene, leading to expression of Cre limited to the MK lineage |
| • The Cxcl4 promoter is a strong driver of Cre expression, leading to high levels of complete inactivation of MK-floxed genes | • In the first-described conditional KOs derived from this construct, valuable insights were obtained because gene ablation only occurred in the MK/platelet lineage with no confounding effects on white cell subsets |
| • There is no loss of native PF4 expression as the Cre is in an inserted BAC clone | |
| Minuses | |
| • There are additional copies of CXC chemokine genes in the inserted BAC clone that alter the observed expression levels of these chemokines, especially in white cells during inflammation | • These mice have only 1 intact copy of the Gp1ba gene, likely affecting MK and platelet biology |
| • The Pf4-Cre construct in a BAC clone causes expression of PF4 in additional hematopoietic lineages (other than MKs) either reflecting the native PF4 expression pattern or due to the nature of the BAC construction | • The Gp1ba-Cre construct may not drive a high Cre level in developing MK with imperfect inactivation of all the copies of a gene in these polyploidic cells |
| Pf4-Cre mice . | Gp1ba-Cre mice . |
|---|---|
| Pluses | |
| • Long prior experience and published literature with this system | • The Cre insert is in the native Gp1ba gene, leading to expression of Cre limited to the MK lineage |
| • The Cxcl4 promoter is a strong driver of Cre expression, leading to high levels of complete inactivation of MK-floxed genes | • In the first-described conditional KOs derived from this construct, valuable insights were obtained because gene ablation only occurred in the MK/platelet lineage with no confounding effects on white cell subsets |
| • There is no loss of native PF4 expression as the Cre is in an inserted BAC clone | |
| Minuses | |
| • There are additional copies of CXC chemokine genes in the inserted BAC clone that alter the observed expression levels of these chemokines, especially in white cells during inflammation | • These mice have only 1 intact copy of the Gp1ba gene, likely affecting MK and platelet biology |
| • The Pf4-Cre construct in a BAC clone causes expression of PF4 in additional hematopoietic lineages (other than MKs) either reflecting the native PF4 expression pattern or due to the nature of the BAC construction | • The Gp1ba-Cre construct may not drive a high Cre level in developing MK with imperfect inactivation of all the copies of a gene in these polyploidic cells |
The pluses and minuses of the previously described Pf4-Cre mice and the Gp1ba-Cre mice based on the present paper and prior literature2,3 are listed.