Fig. 3: p53 is a critical factor in controlling the epigenetic integrity of constitutive heterochromatin, preventing genomic instability.
From: Decoding p53 tumor suppression: a crosstalk between genomic stability and epigenetic control?
Cells lacking functional p53 display altered metabolic status, including a reduction in S-Adenosyl-Methionine (SAM) levels. The reduced availability of SAM impairs the cell’s ability to respond to epigenetic perturbations, as SAM is an essential precursor for the reactions catalyzed by multiple methyl-transferases (MT) that control DNA and histone methylation. The consequential effect of this deregulation is epigenetic instability of constitutive heterochromatin and transcription of repetitive sequences within these genomic regions. Uncontrolled transcription of repetitive sequences disrupts replication progression, leading to genomic instability. Modified from Panatta et al. [40].
