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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Fezf2 overexpression in murine cortical progenitors in vivo

ABSTRACT: Corticospinal motor neurons (CSMN) are one specialized class of cortical excitatory neurons, which connect layer Vb of the cortex to the spinal cord. a master transcription factor –Forebrain expressed zinc finger 2 (Fezf2) – has been identified that is necessary for the fate specification of CSMN. Fezf2 alone can cell-autonomously instruct the acquisition of CSMN-specific features when expressed in diverse, permissive cellular contexts, in vivo. In order to understand the molecular logic underlying the acquisition of CSMN traits upon Fezf2 expression, we compared the in vivo gene expression of FACS-purified cortical progenitors that ectopically expressed Fezf2 to control progenitors. We used in utero electroporation to deliver Fezf2GFP or CtrlGFP expression vectors to neocortical progenitors at E14.5, when they primarily generate CPN of the upper layers. Overexpression of Fezf2 in these progenitors is sufficient to instruct a fate-switch resulting in the generation of CSMN and other subtypes of corticofugal projection neurons. Fezf2GFP- and CtrlGFP -electroporated progenitors were FACS-purified at 24 and 48 hours after surgery and acutely profiled by microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Paola Arlotta

PROVIDER: E-GEOD-56451 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Fezf2 overexpression in murine cortical progenitors in vivo

Project description:Corticospinal motor neurons (CSMN) are one specialized class of cortical excitatory neurons, which connect layer Vb of the cortex to the spinal cord. a master transcription factor –Forebrain expressed zinc finger 2 (Fezf2) – has been identified that is necessary for the fate specification of CSMN. Fezf2 alone can cell-autonomously instruct the acquisition of CSMN-specific features when expressed in diverse, permissive cellular contexts, in vivo. In order to understand the molecular logic underlying the acquisition of CSMN traits upon Fezf2 expression, we compared the in vivo gene expression of FACS-purified cortical progenitors that ectopically expressed Fezf2 to control progenitors.

2014-07-06 | GSE56451 | GEO

E14.5 mouse cortical neurospheres in response to Fezf2 over-expression

Project description:RNA Sequencing of E14.5 mouse cortical neurospheres in response to Fezf2 over-expression 2 replicates each of GFP-transfected or Fezf2/GFP-transfected E14.5 mouse cortical neurospheres. Paired-end sequencing 101bp.

2014-07-06 | E-GEOD-56446 | biostudies-arrayexpress

E14.5 mouse cortical neurospheres in response to Fezf2 over-expression

Project description:RNA Sequencing of E14.5 mouse cortical neurospheres in response to Fezf2 over-expression

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RNA sequencing of corticospinal neurons and control callosal projection neurons purified from the cerebral cortex of adult wild-type and Sod1G86R mice, a model of amyotrophic lateral sclerosis, at four disease-relevant ages.

Project description:Amyotrophic Lateral Sclerosis is clinically defined as the combined degeneration of the corticospinal and corticobulbar neurons (CSN) along with the bulbar and spinal motor neurons (SMN). While a growing body of evidence points to the motor cortex, where CSN are located, as the potential initiation site of ALS, little is known about how CSN degenerate. To gain insights into the molecular mechanisms behind CSN selective degeneration, we first developed an approach to purify this neuronal population from the cerebral cortex of adult wild-type and Sod1G86R mice, combining retrograde labelling and Fluorescence Activated Cell Sorting. In parallel, a second population of cortical neurons, the callosal projection neurons (CPN) located in the layers II/III of the cerebral cortex were also purified. CPN and CSN are both cortical excitatory projection neurons but as opposed to CSN, CPN do not degenerate in Sod1G86R mice, and served as control population. CSN and CPN were purified from same animals, at two presymptomatic ages (3 and 60 days) and two symptomatic ages, 90 and 105 days. A total of 57 samples were further processed and analysed (CSN: 30d: n=4 WT and 3 Sod1G86R; 60d: n=4 WT and 4 Sod1G86R; 90d: n=4 WT and 4 Sod1G86R; 105d: n=4 WT and 2 Sod1G86R; CPN: 30d: n=4 WT and 3 Sod1G86R; 60d: n=2 WT and 3 Sod1G86R; 90d: n=4 WT and 4 Sod1G86R; 105d: n=4 WT and 4 Sod1G86R).

2020-12-30 | E-MTAB-7876 | biostudies-arrayexpress

RNA-seq of postnatal day 0 (P0) wild-type, Fezf2-/- cortices, and Fezf2-/-;Fezf2-EnR cortices

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2021-06-11 | GSE160202 | GEO

Transcription profiling of mouse FACS-purified cortical projection neurons using Affymetrix 430 2.0 microarrays

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2009-10-09 | E-GEOD-17783 | biostudies-arrayexpress

A dynamic unfolded protein response contributes to the control of cortical neurogenesis

Project description:The cerebral cortex contains layers of neurons sequentially generated by distinct lineage-related progenitors. At the onset of corticogenesis, the first-born progenitors are apical progenitors (APs) whose asymmetric division give birth directly to neurons. Later, they switch to indirect neurogenesis by generating intermediate progenitors (IPs), which give rise to projection neurons of all cortical layers. While a direct lineage relationship between APs and IPs has been established, the molecular mechanism that controls their transition remains elusive. Our data suggest that interfering with codon translation speed triggers endoplasmic reticulum stress and the unfolded protein response (UPR), further impairing the generation of IPs and leading to microcephaly. Moreover, we demonstrate that a progressive downregulation of UPR in cortical progenitors acts as physiological signal to amplify IPs and promotes indirect neurogenesis. Thus, our findings reveal a hitherto unrecognized contribution of UPR to cell fate acquisition during mammalian brain development. Ribosome profiling and RNA-Seq of forebrains from E14.5 mouse embryos from wild type animals and mutants carrying a conditional knockout of ELP3 in cortical progenitors

2015-12-11 | E-GEOD-74683 | biostudies-arrayexpress

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Expression data from WT and Fezf2 KO mTECs

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Project description:To investigate the genome-wide binding pattern of Fezf2, we performed ChIP-seq analysis for Fezf2. ChIP-seq of transcription factor in mTECs is difficult because of small number of mTECs or difficulty in gaining ChIP grade antibodies. Then, we generated Fezf2-3Flag knock in mice and performed ChIP-seq analysis by using anti-Flag antibody.

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