First, both coactivators are expressed by developing and mature photoreceptors, and physically interact with the key photoreceptor transcription factor CRX. Second, during photoreceptor development, both factors are found on the promoter/enhancer regions of CRX-regulated photoreceptor genes after CRX binds. These events are followed by acetylation of histone H3 and H4 on these promoters, recruitment of additional photoreceptor-specific transcription factors, and transcriptional activation of the associated genes. Increases in H3 acetylation have also been associated with activation by NRL. Third, in the absence of CRX, recruitment of CBP to target gene promoters and acetylated histone H3/H4 levels are reduced, correlating with decreased transcription. To examine the role of p300/CBP in CRX-regulated photoreceptor gene expression, we conditionally knocked out Ep300 and/or Cbp in rods or cones of the mouse retina using either a rhodopsin or cone opsin promoter to drive Cre recombinase expression. Here we report that loss of both p300 and CBP, but neither alone, causes detrimental defects in rod/cone structure and function, maintenance of photoreceptor gene Artemisinic-acid expression and cell identity. These defects are accompanied by drastically reduced acetylation of histone H3/H4 on photoreceptor genes, and loss of the nuclear chromatin organization pattern characteristic of mouse photoreceptors. During postnatal mouse retinal development between P10 and P21, post-mitotic opsin-positive photoreceptors undergo terminal differentiation and maturation. At the cellular level, they elaborate outer segments containing the phototransduction machinery, and make synaptic connections to inner neurons. At the molecular level, expression of many photoreceptor genes increases to adult levels during this time. These results agree with findings from a study of postmitotic mouse brain neurons, that loss of either p300 or CBP alone does not affect cell viability or cause severe defects. However, these investigators found modest memory and transcriptional deficits after brain-specific knockout of either Ep300 or Cbp.FMOD is a member of the small leucine-rich proteoglycan family and is normally expressed in collagen-rich tissues. We demonstrated that FMOD was expressed at the gene and protein level in CLL and mantle cell lymphoma. This unexpected finding of an aberrantly expressed extracellular matrix protein raised the question whether also other SLRP family members might be expressed in CLL. Overexpression of genes in tumor cells might be due to epigenetic regulations, which may span a cluster of closely located genes. The function of PRELP is unclear, but the interactions between PRELP and collagen type I and II as well as heparin and heparan sulphate suggest that PRELP may be a molecule anchoring basement membranes to connective tissue. Following our previous studies on FMOD and ROR1 in CLL, both located on chromosome 1, the present study was undertaken to explore the gene and protein expression of PRELP in CLL and other hematological malignancies, in our endeavour to explore uniquely expressed molecules in CLL which may play a role in the Glycitin pathobiology of the disease.