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Comparison of retinal gene expression among Chx10-cre Tsc f/f, Chx10-cre Tsc+/+ and 24-month-old C57BL/6 mice

ABSTRACT: Comparison of retinal gene expression among Chx10-cre Tsc f/f, Chx10-cre Tsc+/+ and 24-month-old C57BL/6 mice

PROVIDER: PRJNA736942 | ENA |

REPOSITORIES: ENA

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Comparison of retinal gene expression among Chx10-cre;Tsc f/f, Chx10-cre;Tsc+/+ and 24-month-old C57BL/6 mice

Project description:Retina aging is the main cause of vision decline in elderly population and it is also an important risk factor for the development of degenerative and angiogenic retinal diseases. Therefore it is important to explore the mechanisms which drive retina aging. In this study, we found that retina from old-aged mice had increased mTORC1 activity. Whole transcriptome microarray expression profiling of the retina tissue among among Wild Type Control, Chx10-specific Tsc1 knockout and natural aging mice showed that the most significantly enriched Gene Ontology terms were substantially in common in knockout and aging mice compared to Control mice. we further demonstrated that the activation of mTORC1 in Chx10-expressing cells led to accelerated retina aging and degeneration, with significant functional decline measured by electroretinogram, ganglion cell senescence, microglial cell activation and the accumulation of oxidative stress and inflammatory responses. Inhibition of microglial cells by minocycline partially prevented photoreceptor cell loss and restored the electroretinogram responses. The results demonstrated that mTORC1 activation accelerated retina aging, suggested that microglial cell contributed significantly to overall retinal degeneration.

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Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells tumors

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Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells P21 retinae

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Chromatin accessibility analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells P21 retinae

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Chx10 consolidates V2a interneuron identity through two distinct gene repression modes [RNA-Seq]

Project description:During development, two cell-types born from closely related progenitor pools often express the identical transcriptional regulators despite their completely distinct characteristics. This phenomenon highlights the necessity of the mechanism that operates to segregate the identities of the two cell-types throughout differentiation after initial fate commitment. To understand this mechanism, we investigated the fate specification of spinal V2a interneurons, which share important developmental genes with motor neurons (MNs). Here we demonstrate that the paired homeodomain factor Chx10 functions as a critical determinant for V2a fate and is required to consolidate V2a identity in postmitotic neurons. Chx10 actively promotes V2a fate, downstream of the LIM-homeodomain factor Lhx3, while concomitantly suppressing MN developmental program by preventing the MN-specific transcription complex from binding and activating MN genes. This dual activity enables Chx10 to effectively separate V2a and MN pathways. Together, our study uncovers a widely applicable gene regulatory principle for segregating related cell fates. RNA samples from Chx10-ESC-derived MNs were prepared for sequencing according to the Illumina protocol, and sequenced on the Illumina HiSeq 2000. We will then compare the transcriptome changes between -Dox (no Chx10) and +Dox (Chx10) in order to identify genes rregulated by Chx10.

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Dnmt1 deletion in PV-positive cortical interneurons of 6 month and 18 month old mice [RNA-seq]

2020-07-06 | GSE145025 | GEO

Dnmt1 deletion in PV-positive cortical interneurons of 6 month and 18 month old mice [meDIP-seq]

2020-07-06 | GSE145024 | GEO

Chx10 consolidates V2a interneuron identity through two distinct gene repression modes [ChIP-Seq]

Project description:During development, two cell-types born from closely related progenitor pools often express the identical transcriptional regulators despite their completely distinct characteristics. This phenomenon highlights the necessity of the mechanism that operates to segregate the identities of the two cell-types throughout differentiation after initial fate commitment. To understand this mechanism, we investigated the fate specification of spinal V2a interneurons, which share important developmental genes with motor neurons (MNs). Here we demonstrate that the paired homeodomain factor Chx10 functions as a critical determinant for V2a fate and is required to consolidate V2a identity in postmitotic neurons. Chx10 actively promotes V2a fate, downstream of the LIM-homeodomain factor Lhx3, while concomitantly suppressing MN developmental program by preventing the MN-specific transcription complex from binding and activating MN genes. This dual activity enables Chx10 to effectively separate V2a and MN pathways. Together, our study uncovers a widely applicable gene regulatory principle for segregating related cell fates. ChIP DNA samples from Chx10-ESC-derived MNs were prepared for sequencing according to the Illumina protocol, and sequenced on the Illumina HiSeq 2000. The peak calling was conducted with MACS software (Zhang et al., 2008). MEME-ChIP Suite (Bailey et al., 2009; Machanick and Bailey, 2011) and TOMTOM algorithm (Gupta et al., 2007) was used for motif analysis.

2016-07-28 | E-GEOD-83872 | biostudies-arrayexpress

Next Generation Sequencing Analysis of livers from 2-month WT/12-month WT and 2-month HKO/12-month nontumor/12month- tumor.

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2020-05-05 | GSE130745 | GEO

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