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GCN5 Functions in Telomere Maintenance and Neural Development

We reported previously GCN5 deletion in the mouse leads to embryonic lethality due to increased apoptosis. New data show that this apoptosis is p53 dependent and may be triggered by telomere defects. Telomeres are shortened in cells from GCN5 mutant embryos, and these cells display increased numbers of chromosomal end associations and fusions. In the absence of both p53 and GCN5, an even greater incidence of telomere fusion is observed. These double mutant embryos also display defects in neural tube closure and brain development. Very similar defects in neural development are observed in mice homozygous for GCN5 HAT catalytic site mutations and in mice that carry a hypomorphic allele of GCN5. These data provide the first evidence that GCN5 may be required both for telomere maintenance and proper expression of genes required for neural development in the mouse.