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Table 4 Cardiovascular defects in second heart field mutant embryos and neonates

From: Msx1 haploinsufficiency modifies the Pax9-deficient cardiovascular phenotype

Genetic background—genotype and stage

n

VSD

DORV + IVC

cAo

IAA-B ± A-RSA

A-RSA

Absent CC

B6-Pax9ΔSHF

E15.5

9

1/9 (11%)

5/9 (56%)

1/9 (11%)

8/9 (89%)

1/9 (11%)

9/9 (100%)

CD1-Pax9ΔSHF

Neonate

1

N/A

N/A

0

1

0

1

CD1-Pax9ΔSHF;Msx1+/–

Neonate

8

0

0

2/8 (25%)

0

2/8 (25%)

0

  1. All mice with Pax9 conditionally inactivated from the second heart field with Isl1Cre (Pax9ΔSHF) had pre-axial digit duplication, absent thymus and normal palate. N/A, not assessed
  2. 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
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BMC Developmental Biology

ISSN: 1471-213X

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