Mature rod photoreceptor cells contain very small nuclei with tightly condensed 
heterochromatin. We observed that during mouse rod maturation, the nucleosomal 
repeat length increases from 190 bp at postnatal day 1 to 206 bp in the adult 
retina. At the same time, the total level of linker histone H1 increased 
reaching the ratio of 1.3 molecules of total H1 per nucleosome, mostly via a 
dramatic increase in H1c. Genetic elimination of the histone H1c gene is 
functionally compensated by other histone variants. However, retinas in 
H1c/H1e/H1(0) triple knock-outs have photoreceptors with bigger nuclei, 
decreased heterochromatin area, and notable morphological changes suggesting 
that the process of chromatin condensation and rod cell structural integrity are 
partly impaired. In triple knock-outs, nuclear chromatin exposed several 
epigenetic histone modification marks masked in the wild type chromatin. 
Dramatic changes in exposure of a repressive chromatin mark, H3K9me2, indicate 
that during development linker histone plays a role in establishing the 
facultative heterochromatin territory and architecture in the nucleus. During 
retina development, the H1c gene and its promoter acquired epigenetic patterns 
typical of rod-specific genes. Our data suggest that histone H1c gene expression 
is developmentally up-regulated to promote facultative heterochromatin in mature 
rod photoreceptors.