Table 3.

Key genetic and epigenetic modifiers encoded on chr. 22q11.2

Gene name (protein name if coding)Gene functionMechanism of actionClinical phenotypesComparative mouse modelsa
TBX1 (T-box transcription factor 1) Transcription factor Binds DNA sequences and associates with histone methyltransferases to activate transcription Multiple and variable congenital defects (see Table 1) KOb is embryonic lethal
Haploinsufficiency: Similar phenotypes as humans but much less penetrant thymic hypoplasia 
CRKL (CRK-like) SH2 and SH3 domain containing intracellular signaling adapter protein Promotes intracellular signal transduction Genetic modifier of 22q11.2DS KO is prenatal lethal with heart, liver, and placental defects
Crkl+/−Tbx1+/− mice: CHDc and thymic hypoplasia 
CLDN 5 (CLAUDIN 5) Tight junction protein Blood–brain barrier (BBB) integrity
Cortical thymus–blood barrier 
Increased vascular permeability and weakened BBB Mouse KO leads to nonviable offspring due to defective BBB 
DGCR6 (DGCR6) Nuclear phosphoprotein Expressed in neural crest cells
Homology to laminin-g1 chain 
CHD with deletion or duplication Haplosufficiency associated with learning deficit 
DGCR8 (DGCR8) MicroRNA processing enzyme Required for miRNA biogenesis Processing microRNAs in immune cells and neural progenitors KO is embryonic lethal at E6.5 
MiR-185 MicroRNA Targets SERCA2, BTK, MZB1, NFAT, CAM4K Potential contributor to autoantibody production KO is normal: Increased bone formation during osteogenesis
Haploinsufficiency correlated with increased autoantibody 
DGCR5 LncRNA Regulator of alternative splicing Unknown No mouse model 
Gene name (protein name if coding)Gene functionMechanism of actionClinical phenotypesComparative mouse modelsa
TBX1 (T-box transcription factor 1) Transcription factor Binds DNA sequences and associates with histone methyltransferases to activate transcription Multiple and variable congenital defects (see Table 1) KOb is embryonic lethal
Haploinsufficiency: Similar phenotypes as humans but much less penetrant thymic hypoplasia 
CRKL (CRK-like) SH2 and SH3 domain containing intracellular signaling adapter protein Promotes intracellular signal transduction Genetic modifier of 22q11.2DS KO is prenatal lethal with heart, liver, and placental defects
Crkl+/−Tbx1+/− mice: CHDc and thymic hypoplasia 
CLDN 5 (CLAUDIN 5) Tight junction protein Blood–brain barrier (BBB) integrity
Cortical thymus–blood barrier 
Increased vascular permeability and weakened BBB Mouse KO leads to nonviable offspring due to defective BBB 
DGCR6 (DGCR6) Nuclear phosphoprotein Expressed in neural crest cells
Homology to laminin-g1 chain 
CHD with deletion or duplication Haplosufficiency associated with learning deficit 
DGCR8 (DGCR8) MicroRNA processing enzyme Required for miRNA biogenesis Processing microRNAs in immune cells and neural progenitors KO is embryonic lethal at E6.5 
MiR-185 MicroRNA Targets SERCA2, BTK, MZB1, NFAT, CAM4K Potential contributor to autoantibody production KO is normal: Increased bone formation during osteogenesis
Haploinsufficiency correlated with increased autoantibody 
DGCR5 LncRNA Regulator of alternative splicing Unknown No mouse model 
a

Phenotypic differences exist in strains used.

b

Knockout.

c

Congenital Heart Disease

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