Table 1.

Representative Analyses of Marker Genes Used for Bone Marrow and Skeletal Stem Cell Identities

Mouse Strains	Major Descriptions	Authors' Comments	References
Col2.3-GFP transgenic mice	express GFP in osteoblasts and osteocytes under the control of the 2.3-kb rat Col 1a1 (procollagen, type 1, alpha 1) promoter	useful for studying bone development and osteoblast lineage tracing; wary of rat subspecies sequence effects	Kalajzic et al., 2002
Cxcl12-dsRed	▸express dsRedE2 from the mouse endogenous Cxcl12 promoter ▸the dsRed knockin produces a strong loss-of-function allele ▸dsRed recognized by anti-RFP	useful for identifying Cxcl12-expressing perivascular stromal cells and endothelial cells in the bone marrow	Ding and Morrison, 2013
Cxcl12-GFP knockin mice	highly enriched in Cxcl12-abundant reticular (CAR) cells within the intra-trabecular space in the bone marrow	endothelial cells and the endosteal surface osteoblasts show faint or undetectable GFP signals	Ara et al., 2003, Sugiyama et al., 2006
Gt(ROSA)26Sortm1(HBEGF)Awai	▸have the simian diphtheria toxin receptor (DTR; from simian Hbegf) inserted into the Gt(ROSA)26S or the ROSA26 locus, whose expression is suppressed by an upstream loxP-flanked STOP sequence ▸inducible expression of DTR by Cre recombinase	suitable for ablation of cells that express DTR following diphtheria toxin treatment	Buch et al., 2005
Leprfl/fl	B6.129P2-Leprtm1Rck/J, also known as: ObRFlox ▸ have loxP sites on either side of exon 1 of the mouse Lepr gene ▸ delete exon 1 when bred to a Cre recombinase-expressing mice under a tissue-specific promoter	▸useful in studies of obesity and Lepr related cell lineage analysis ▸beware of expression of short Lepr isoforms that are initiated after exon 1	Cohen et al., 2001 http://www.jax.org/
Lepr-Cre	L B6.129-Leprtm2(Cre)Rck/J (Lepr-Cre); the targeting vector contains an IRES-NLS-Cre and a neo (flanked by frt sites) inserted immediately 3′ of the stop codon in the last exon of the Lepr gene	transcripts may terminate in many Lepr transcript variants that do not contain the last exon of the canonical Lepr isoform (Lepr-B)	DeFalco et al., 2001
Mx-1-Cre, transgenic mice	B6.Cg-Tg(Mx1-cre)1Cgn/J, also known as Mx-Cre and Mx1-Cre (BALB/c): the Mx-1-Cre transgene contains Cre recombinase under the control of the Mx-1 promoter that is silent in healthy mice	▸the Mx-1 promoter is highly sensitive to interferon α/β and synthetic double-stranded RNAs, e.g., poly(I:C) ▸cautions should be taken when experimental conditions involving interferons and exogenous double-stranded RNAs	Kuhn et al., 1995 http://www.jax.org/
Nes-Cre	Cre recombinase is expressed under the control of the 5.8-kb rat Nes promoter and the 1.8-kb intron 2 enhancer element	▸no ERT2 fragment in the construct ▸genomic orientation of the Nes genomic elements is similar to that of Nes-GFP described by Mignone et al. (2004)	Tronche et al., 1999
Nes-CreERT2 transgenic mice	C57BL/6-Tg(Nes-cre/ERT2)KEisc/J: ▸ express the T2 mutant form of a Cre-estrogen receptor fusion (Cre-ERT2) under the control of the 1.8-kb rat Nes intron-2 enhancer (i2E) element and a 160-bp HSV TK promoter followed by an SV40 polyA site ▸ Cre-ERT2 fusion protein activity: inducible to the nucleus at high levels following binding of tamoxifen, which deletes the floxed sequences in cells of bred mice ▸ the Nes-CreERT2 transgene directs Cre expression in Nes-expressing cells in the subventricular zone (SVZ) and subgranular zone (SGZ) ▸ useful for studying the lineage commitments in both adult and developing mouse brains	▸the 4.2-kb transgene fragment excluded the majority of the rat 5′ promoter sequence ▸the intron-2 enhancer element orientated differently from that of the Nes-GFP construct (Mignone et al., 2004); thus may have differential transcriptional effects ▸a complicated inducible system, involving mixed estrogen-agonist effects of tamoxifen on the impairment of bone growth, apoptosis in growth plate chondrocytes in cultured rat metatarsal bones, and signal transductions between endothelial cells and pericytes	Balordi and Fishell, 2007, Chagin et al., 2007, Feil et al., 1997, Karimian et al., 2008, Lagace et al., 2007, Zimmerman et al., 1994
Nes-GFP	Tg(Nes-EGFP)33Enik: a Nes-GFP reporter in transgenic mice, driven by the 5.8 promoter and 1.8-kb intron 2 enhancer of the rat Nes gene	▸predicting CNS neural stem cell or progenitor specific promoter and intron 2 enhancer transcriptional activity ▸rat sequence in a mouse model ▸expected differences among Nes-GFP, Nes-Cre, and Nes-CreERT2 strains	Lendahl et al., 1990, Mignone et al., 2004, Zimmerman et al., 1994
NG2-CreER™	B6.Cg-Tg(Cspg4-Cre/Esr1∗)BAkik/J, ▸ NG2-CreER™ BAC transgenic mice ▸ tamoxifen-inducible Cre (CreER™) under the control of the mouse NG2 (Cspg4) promoter/enhancer	useful for inducible Cre recombinase expression in NG2-expressing glia and other cell types	Zhu et al., 2011; http://www.jax.org/
P0-Cre	transgenic mice expressing Cre recombinase directed by the myelin protein zero (P0) gene promoter	genetic tools for labeling neural crest cell lineages such as Schwann cells	Feltri et al., 1999, Yamauchi et al., 1999
Prx1-Cre	B6.Cg-Tg(Prrx1-cre)1Cjt/J: expresses Cre under the control of a Prrx1-derived enhancer	useful for studying limb bud development and patterning	Logan et al., 2002
Wnt1-Cre	▸carrying Cre cDNA between Wnt1 promoter and enhancer ▸widely used in the study of brain development, the neural crest and its derivatives	▸phenotypes can be complicated by ectopic activation of canonical Wnt/β-catenin signaling related to increased Wnt1 protein expression ▸may be used as a gain-of-function model for studying Wnt signaling mechanisms in middle brain development	Danielian et al., 1998, Lewis et al., 2013
Wnt1-Cre2	Cre expression under the control by 1.3-kb 5′ promoter and 5.5-kb 3′ enhancer	▸serve similar purposes to the original Wnt1-Cre (Danielian et al., 1998) ▸deprived of complicated phenotypes associated with gain of function of Wnt1	Lewis et al., 2013

Cre, Cre recombinase; Cxcl12, chemokine (C-X-C motif) ligand 12; GFP, green fluorescent protein; HSV, herpes simplex virus; IRES, internal ribosome entry site; Neo, neomycin resistance gene; NLS, nuclear localization signal; RFP, red fluorescent protein; TK, thymidine kinase.