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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Comparison of the retinal transcriptomes of four Bhlhe23-/- mice and 4 sex and litter-matched wild type mice

ABSTRACT: Bhlhe23 is a transcription factor that is required for the maturation and survival of retinal rod bipolar cells in mice. In the adult Bhlhe23-/- retina, rod bipolar cells are almost completely absent. We identified genes that were likely to be important to rod bipolar cell maintenance and function by identifying genes that were significantly down-regulated in the transcriptome of adult Bhlhe23-/- mouse retina compared with wild type retina.

ORGANISM(S): Mus musculus

SUBMITTER: Sasha Woods

PROVIDER: E-MTAB-6069 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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RNA-seq of retina from 6 pairs of litter-matched Bhlhe23-/- and wild type mice at postnatal day 7

Project description:Bhlhe23 is a transcription factor that is required for the maturation and survival of retinal rod bipolar cells in mice. In the Bhlhe23-/- retina, rod bipolar cells are born in normal numbers, then die by apoptosis from postnatal day 8. We identified genes that were likely to be important to rod bipolar cell development and survival by identifying genes that were significantly differentially expressed in the transcriptome of the Bhlhe23-/- mouse retina compared with wild type retina at postnatal day 7. just before the onset of rob bipolar cell death.

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Project description:Microarray analysis on total retinal RNA from 15 day old Sirt6 wild-type (WT) and knock-out (KO) mice. The retina is one of the major energy consuming tissues within the body. In this context, synaptic transmission between light-excited rod photoreceptors and downstream ON-bipolar neurons is a highly demanding energy consuming process. Sirtuin 6 (SIRT6), a NAD-dependent deacylase, plays a key role in regulating glucose metabolism. In this study, we demonstrate that SIRT6 is highly expressed in the retina, controlling levels of histone H3K9 and H3K56 acetylation. Notably, despite apparent normal histology, SIRT6 deficiency caused major retinal transmission defects concomitant to changes in expression of glycolytic genes and glutamate receptors, as well as elevated levels of apoptosis in inner retina cells. Our results identify SIRT6 as a critical modulator of retinal function, likely through its effects on chromatin. Microarray analysis of total retinal RNA from 15 day old Sirt6 wild-type (WT) and knock-out (KO) mice with 3 replicates in each condition using the Affymetrix Mouse Gene 2.1 ST array (transcript (gene) version).

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