Post-translational modifications of histone amino termini are an important 
regulatory mechanism that induce transitions in chromatin structure, thereby 
contributing to epigenetic gene control and the assembly of specialized 
chromosomal subdomains. Methylation of histone H3 at lysine 9 (H3-Lys9) by 
site-specific histone methyltransferases (Suv39h HMTases) marks constitutive 
heterochromatin. Here, we show that H3-Lys9 methylation also occurs in 
facultative heterochromatin of the inactive X chromosome (Xi) in female mammals. 
H3-Lys9 methylation is retained through mitosis, indicating that it might 
provide an epigenetic imprint for the maintenance of the inactive state. 
Disruption of the two mouse Suv39h HMTases abolishes H3-Lys9 methylation of 
constitutive heterochromatin but not that of the Xi. In addition, HP1 proteins, 
which normally associate with heterochromatin, do not accumulate with the Xi. 
These observations suggest the existence of an Suv39h-HP1-independent pathway 
regulating H3-Lys9 methylation of facultative heterochromatin.