Molecular Vision: Tummala, Mol Vis 2010; 16:252-271. Table 5

Table 5. Some examples of gene activation increases predicted by Pol-II ChIP-on-Chip, which have human homologs located in mapped intervals of unidentified retinal diseases.

Human disease (location)	Human gene name	Pol-II peak signal ratio mouse homolog (P25/P2)	mRNA expression P2 versus P25 mouse neural retina (±SD, n=3)		mRNA expression normal versus Rd1 mouse neural retina (±SD, n=3)
Human disease (location)	Human gene name	Pol-II peak signal ratio mouse homolog (P25/P2)	P2	P25	Normal (P33)	Rd1 (P33)
LCA9(1p36)	SLC25A33	2	1.00±0.07	7.1±0.1†	1.00±0.06	0.49±0.01†
MCDR3(5p15.33-p13.1)	LPCAT1	2.2	1.00±0.03	3.5±0.4†	1.00±0.01	0.55±0.05†
MDDC, CYMD (7p21-p15)	CCDC126	3.2	1.0±0.1	26.1±0.2†	1.00±0.04	0.09±0.03†
CORD4(17q) ‡	ARL4D	3.6	1.0±0.2	127±11†	1.00±0.04	0.12±0.01†

Pol-II peak signal ratios (P25/P2) are derived from ChIP-on-Chip data and predicted gene activation (≥1.8). Relative gene expression was then examined by real time PCR (Taqman) comparing P25 and P2 normal retina. Gene expression was also compared between normal retinas (P33) and Rd1 retinas (P33) that had lost >99.7% of their rod-photoreceptors. † p<0.001, t-test. LCA9 (recessive Leber congenital amaurosis, Type 9); MCDR3 (dominant macular dystrophy-3); MDDC, CYMD (dominant macular dystrophy cystoid); CORD4 (cone rod dystrophy) ‡ location by estimation, not yet mapped.