TABLE 1

Genetically modified mouse models to study Ackr3 expression in vivo and associated phenotypes

Model	Genetic Background	Description	References
Constitutive deletion
Ackr3^−/−	C57Bl/6	Mice carrying loxP-flanked Ackr3 exon 2 crossed with Deleter-Cre mice	Sierro et al. (2007), Sánchez-Alcañiz et al. (2011), Wang et al. (2011), Yu et al. (2011), Trousse et al. (2015)
		Phenotype: Perinatal death of >95% Ackr3^−/− mice.
		Thickened semilunar valves. Normal development of B cells and granulocytes. Altered neuron migration during embryonic development.
Ackr3^−/−	129 Sv/Ev x C57Bl/6	Knock-in of LacZ reporter in Ackr3 exon 2 (IRES-LacZ/PGK- Neo cassette)	Gerrits et al. (2008)
		Phenotype: Perinatal death of 70% Ackr3⁻^/− mice.
		Nonviable mice: Myocardial degeneration, fibrosis, and cardiac hyperplasia. No defects in semilunar valves.
		Surviving mice: Cardiac hyperplasia in 25%. Normal lifespan, no hematopoietic or hematologic defects, no reproductive defects.
Conditional (tissue- or cell type–specific) deletion
Tie2-Cre; Ackr3^flox/−	C57Bl/6	Endothelium-specific deletion.	Sierro et al. (2007), Yu et al. (2011)
		Phenotype: Mice survive to adulthood and are fertile.
		Cardiac hypertrophy, thickened ventricular walls, and thickened semilunar valves in 40% of the mice.
Dlx5/6-Cre; Ackr3^flox/flox	C57Bl/6	GABAergic neuron-specific deletion.	Sánchez-Alcañiz et al. (2011)
Dlx5/6-Cre; Ackr3^flox/flox	C57Bl/6	Phenotype: Mice survive to adulthood. Altered migration of neurons during embryonic development (E16.5).	Sánchez-Alcañiz et al. (2011)
DlxI12b-Cre; Ackr3^flox/−	C57Bl/6 CD1	GABAergic neuron-specific deletion.	Wang et al. (2011)
DlxI12b-Cre; Ackr3^flox/−	C57Bl/6 CD1	Phenotype: Neuron positioning defects similar to those of constitutive Ackr3 ⁻^/− mice.	Wang et al. (2011)
Emx1-Cre; Ackr3^flox/−	Not given	Glutamatergic neuron-specific deletion.	Wang et al. (2011)
Emx1-Cre; Ackr3^flox/−	Not given	Phenotype: No effect on the position of cortical projection neurons.	Wang et al. (2011)
Tbr2-Cre; Ackr3^flox/flox	Not given	Glutamatergic neuronal progenitor-specific deletion. Phenotype: Altered migration of neurons in adulthood.	Abe et al. (2018)
Dbx1-Cre; Ackr3^flox/flox	C57Bl/6	Cajal-Retzius neuron progenitor-specific deletion.	Trousse et al. (2015)
Dbx1-Cre; Ackr3^flox/flox	C57Bl/6	Phenotype: Defects in the positioning of a subpopulation of Dbx1-expressing neurons during embryonic development (E14.5).	Trousse et al. (2015)
Conditional-inducible (cell type-specific inducible) deletion
Scl-Cre^ERT; Ackr3^flox	C57Bl/6	Tamoxifen-inducible deletion of Ackr3 from Scl-expressing cells (HSC, myeloid lineage, endothelium and regions in the central nervous system) in adult mice.	Stacer et al. (2016)
Scl-Cre^ERT; Ackr3^flox	C57Bl/6	Findings: ∼35% increase in CXCL12 plasma levels. No other apparent phenotype described.	Stacer et al. (2016)
Reporter gene
Ackr3^+/EGFP	C57Bl/6	Replacement of Ackr3 exon 2 by EGFP. No phenotype is described.	Cruz-Orengo et al. (2011)
Ackr3-EGFP	CD1	BAC insertion of the Ackr3 promoter fused to an EGFP coding region. Endogenous Ackr3 locus remains intact. No secondary effects.	The Gene Expression Nervous System Atlas (GENSAT)
Ackr3-EGFP	CD1		Gong et al. (2003)