. 2021 Oct 6;21:14. doi: 10.1186/s12861-021-00245-5

Table 4.

Cardiovascular defects in second heart field mutant embryos and neonates

Genetic background—genotype and stage	n	VSD	DORV + IVC	cAo	IAA-B ± A-RSA	A-RSA	Absent CC
B6-Pax9^ΔSHF E15.5	9	1/9 (11%)	5/9 (56%)	1/9 (11%)	8/9 (89%)	1/9 (11%)	9/9 (100%)
CD1-Pax9^ΔSHF Neonate	1	N/A	N/A	0	1	0	1
CD1-Pax9^ΔSHF;Msx1^+/– Neonate	8	0	0	2/8 (25%)	0	2/8 (25%)	0

Genetic background—genotype and stage

VSD

DORV + IVC

cAo

IAA-B ± A-RSA

A-RSA

Absent CC

B6-Pax9^ΔSHF

E15.5

1/9 (11%)

5/9 (56%)

1/9 (11%)

8/9 (89%)

1/9 (11%)

9/9 (100%)

CD1-Pax9^ΔSHF

Neonate

N/A

CD1-Pax9^ΔSHF;Msx1^+/–

Neonate

2/8 (25%)

All mice with Pax9 conditionally inactivated from the second heart field with Isl1Cre (Pax9^ΔSHF) had pre-axial digit duplication, absent thymus and normal palate. N/A, not assessed

A-RSA, aberrant right subclavian artery; cAo, cervical aorta; CC, common carotid artery; DORV + IVC, double outlet right ventricle with interventricular communication; IAA,-B interrupted aortic arch type B; SHF, second heart field; VSD, perimembranous ventricular septal defect