Proximal 445 bp of the mouse SM22α (Tagln) gene promoter. In transgenic mice it reproduces the embryonic expression pattern of endogenous SM22α in cardiac, skeletal, and vascular smooth muscle lineages, then becomes restricted postnatally to conductive arterial smooth muscle, notably excluding venous and visceral smooth muscle despite endogenous SM22α expression there.
Length: 2960 bp
Strength: moderate
Tissue: Embryonic cardiac, skeletal muscle, and vascular smooth muscle lineages; postnatally restricted to conductive arterial smooth muscle (aorta and major arteries), excluding venous and visceral smooth muscle despite endogenous SM22α expression there (Li et al. 1996)
Expression: developmental
Origin: Mouse (Mus musculus) Tagln/SM22α gene
Characteristics
Contains two CArG boxes (at -150 and -274 relative to the transcription start site) required for smooth-muscle-specific transcription; deleting the promoter to -144 bp reduces reporter activity roughly sixfold in primary rat aortic smooth muscle cells (Li et al. 1996). In transgenic mice, the fragment reproduces the embryonic temporospatial pattern of endogenous SM22α — appearing in the primitive heart tube by E8.75, marking the dorsal aorta by E9.0, and progressively labeling conductive arterial vessels through E14.5 — and is roughly threefold more active in aortic smooth muscle cells than in 10T1/2 fibroblasts, while inactive in F9 teratocarcinoma cells (Li et al. 1996).
Applications: Used in transgenic reporter and Cre-recombinase constructs to target gene expression or lineage tracing to conductive arterial vascular smooth muscle cells while sparing visceral and venous smooth muscle, suited to studies of arterial biology, atherosclerosis, and vascular remodeling (Li et al. 1996).
Limitations: Restricted to conductive arterial smooth muscle among smooth muscle subtypes — inactive in venous smooth muscle and in visceral smooth muscle of the gut, stomach, bladder, and bronchi, despite endogenous SM22α expression in those tissues (Li et al. 1996). Also directs expression in cardiac and skeletal muscle lineages during embryogenesis, which can produce non-vascular off-target expression if assayed before E14.5 (Li et al. 1996).
Li et al. (1996).
Expression of the SM22alpha promoter in transgenic mice provides evidence for distinct transcriptional regulatory programs in vascular and visceral smooth muscle cells.
J Cell Biol - Li 1996 SM22a Promoter Specificity
Choosing a selection results in a full page refresh.
