Skip to main content
. 2018 Dec 16;2018:8908751. doi: 10.1155/2018/8908751

Table 2.

Involvement of HAT in normal development.

HAT Organism Impact on development Ref
CBP Null mice Neural tube closure and embryonic vascular and cardiac defects [35]

CBP Mice harbouring point mutation or deletion of the HAT domain Several defects in memory and synaptic plasticity [37, 38]

CBP Null mice Rubinstein-Taybi syndrome (RTS) multilineage [8]

p300 Heterozygous mice Embryonic lethality [35]

p300 Mice harbouring point mutation Defects in the hematopoiesis (B-cell deficiency, megakaryocytosis, and thrombocytosis) [39]

GCN5 Mice harbouring a point mutations abrogating GN5 HAT activity Cranial neural tube closure defects and exencephaly [41]

GCN5 Null mice Early embryonic lethality [40]
Knockdown zebrafish Cardiac, fin, and limb defects [45]

pCAF Null mice Normal phenotype in the embryo [42, 44]
Defects in learning abilities and short-term and long-term memory in adult [44]
Knockdown zebrafish Cardiac, fin, and limb defects [45]

ATAT-1 Null mice Viable, without morphological defects; loss of α-tubulin acetylation in sperm flagella; dentate gyrus distortion [46]