Table 1.

Mouse models of SRF ablation with embryonic lethality

Embryonic day	Key heart characteristics	SRF KO Mutant	Consequences	Lethality	References
–	–	SRF null	• No change till E6.5	E8.5	[23, 42]
			• Small embryo
			• Delayed development
			• Inability to form Primitive Streak
			• No mesodermal cells
			• pr. of Pykontic TUNEL positive cells
			• Impaired Gastrulation
			• Fscn1↓, Crk1↓
E 7.5–8.0	Fusion and formation of a single beating heart tube	Nkx 2.5 Cre	• Lack of Beating cells	–	[24]
			• Impaired sarcomerogenesis
			• Hampered miRNA activity
			• Cardiac α-actin ↓
			• GATA 6 ↑, BMP4 ↑
			• KCNMB1 ↓
		βMHC Cre	• Sarcomerogenesis ↓	E10.5–13.5	[18]
			• Cell Survival ↓
			• Apoptosis ↑
			• Blood accumulation
			• Enlarged ventricular lumen
			• Impaired cell–cell interaction
		αMHC Cre	• Chamber dilation	E11.5	[25]
			• Cardiac insufficiency
			• Poorly developed interventricular groove
			• Sarcomere organization ↓
			• Apoptosis ↑
			• Cardiac, skeletal, SMC α-actin ↓
			• heartbeat stops around E11.5
E 8.5–9.0	Heart tube undergoes looping followed by bulging of the heart regions	SM22α Cre	• Normal till E8.5	E11.5	[19]
			• Restricted growth
			• Abnormal cardiac trabeculation
			• Reduced vascular SMC recruitment to the dorsal aorta
	Instrumentation of regular heart beat		• Disorganised cardiac sarcomere
			• Loss of intermediate filament bundles in vascular SMC
			• Compromised Z disc structure

This table summarizes various SRF deletion mouse models at different embryonic stages. Constitutive as well as developmental stage-specific deletion of SRF using specific promoter Cre lines resulted in lethal defects suggesting the indispensable role SRF plays during embryonic development

KCNMA1; Potassium Calcium-Activated Channel Subfamily M Alpha 1, pr; presence, Crk; chicken tumour virus no. 10 [CT10] regulator of kinase, FSCN1; Fascin Actin-Bundling Protein 1