Fez family transcription factors: Controlling neurogenesis and cell fate in the developing mammalian nervous system

Eckler, Matthew J.; Chen, Bin

doi:10.1002/bies.201400039

Cited by 38 publications

(43 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Given that Notch has conserved roles in regulating mammalian NSC self-renewal and heterogeneity and that Fezf1/2, which are homologs of Erm, are also expressed in mammalian NSCs and regulate neurogenesis and NSC activation/ quiescence (Berberoglu et al, 2014;Eckler and Chen, 2014;Guo et al, 2013), it would be of great interest to investigate if similar mechanisms are conserved in mammalian NSCs.…”

Section: Discussionmentioning

confidence: 99%

Notch maintains Drosophila type II neuroblasts by suppressing the expression of the Fez transcription factor Earmuff

Xie

Zhu

2016

Development

View full text Add to dashboard Cite

Notch signaling is crucial for maintaining neural stem cell (NSC) selfrenewal and heterogeneity; however, the underlying mechanism is not well understood. In Drosophila, loss of Notch prematurely terminates the self-renewal of larval type II neuroblasts (NBs, the Drosophila NSCs) and transforms type II NBs into type I NBs. Here, we demonstrate that Notch maintains type II NBs by suppressing the activation of earmuff (erm) by Pointed P1 (PntP1). We show that loss of Notch or components of its canonical pathway leads to PntP1-dependent ectopic Erm expression in type II NBs. Knockdown of Erm significantly rescues the loss-of-Notch phenotypes, and misexpression of Erm phenocopies the loss of Notch. Ectopically expressed Erm promotes the transformation of type II NBs into type I NBs by inhibiting PntP1 function and expression in type II NBs. Our work not only elucidates a key mechanism of Notch-mediated maintenance of type II NB self-renewal and identity, but also reveals a novel function of Erm.

show abstract

Section: Discussionmentioning

confidence: 99%

Notch maintains Drosophila type II neuroblasts by suppressing the expression of the Fez transcription factor Earmuff

Xie

Zhu

2016

Development

View full text Add to dashboard Cite

show abstract

“…TBR1 binds to a 3′ region of the Fezf2 gene and directly represses high-level Fezf2 expression in layer 6 neurons (9, 11). Thus, the expression level of Fezf2 is precisely regulated in the developing cortex for proper specification of subcerebral and corticothalamic neuronal fates (14,15).…”

mentioning

confidence: 99%

Mutual regulation between Satb2 and Fezf2 promotes subcerebral projection neuron identity in the developing cerebral cortex

McKenna

Ortiz-Londono

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

View full text Add to dashboard Cite

Generation of distinct cortical projection neuron subtypes during development relies in part on repression of alternative neuron identities. It was reported that the special AT-rich sequencebinding protein 2 (Satb2) is required for proper development of callosal neuron identity and represses expression of genes that are essential for subcerebral axon development. Surprisingly, Satb2 has recently been shown to be necessary for subcerebral axon development. Here, we unravel a previously unidentified mechanism underlying this paradox. We show that SATB2 directly activates transcription of forebrain embryonic zinc finger 2 (Fezf2) and SRY-box 5 (Sox5), genes essential for subcerebral neuron development. We find that the mutual regulation between Satb2 and Fezf2 enables Satb2 to promote subcerebral neuron identity in layer 5 neurons, and to repress subcerebral characters in callosal neurons. Thus, Satb2 promotes the development of callosal and subcerebral neurons in a cell context-dependent manner.Satb2 | Fezf2 | subcerebral neurons | cerebral cortex | cell fate P rojection neurons in the six-layered neocortex can be classified based on axonal projections. The corticocortical neurons send axons to other areas in the ipsilateral cortex or through the corpus callosum and into the contralateral cortex (i.e., callosal projection neurons). The callosal neurons are distributed throughout layers 2-6, but are most abundant in layers 2 and 3. The corticofugal neurons consist of corticothalamic and subcerebral neurons. The corticothalamic neurons are most abundant in layer 6, and send axons into the thalamus. The subcerebral neurons are located in layer 5, and project axons into the spinal cord, superior colliculus, pons, and other brain areas (1-4).

show abstract

“…FEZF2 is a conventional transcription factor highly conserved in vertebrate organisms and first identified for its roles in neurogenesis, cell‐fate specification, and axon guidance . In TECs, FEZF2 expression is detected during embryogenesis and increases until the perinatal period.…”

Section: Transcription Factors Involved In Central Tolerancementioning

confidence: 99%

AIRE: a missing link to explain female susceptibility to autoimmune diseases

Berrih‐Aknin

Panse

Dragin

2017

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

Women are more susceptible to autoimmune diseases than men. Autoimmunity results from tolerance breakdown toward self-components. Recently, three transcription modulators were identified in medullary thymic epithelial cells that orchestrate immune central tolerance processes: the autoimmune regulator (AIRE), FEZ family zinc finger 2 (FEZF2 or FEZ1), and PR domain zinc finger protein 1 (PRDM1). Interestingly, these three transcription modulators regulate nonredundant tissue-specific antigen subsets and thus cover broad antigen diversity. Recent data from different groups demonstrated that sex hormones (estrogen and testosterone) are involved in the regulation of thymic AIRE expression in humans and mice through direct transcriptional modulation and epigenetic changes. As a consequence, AIRE displays gender-biased thymic expression, with females showing a lower expression compared with males, a finding that could explain the female susceptibility to autoimmune diseases. So far, FEZF2 has not been related to an increased gender bias in autoimmune disease. PRDM1 expression has not been shown to display gender-differential thymic expression, but its expression level and its gene polymorphisms are associated with female-dependent autoimmune disease risk. Altogether, various studies have demonstrated that increased female susceptibility to autoimmune diseases is in part a consequence of hormone-driven reduced thymic AIRE expression.

show abstract

Fez family transcription factors: Controlling neurogenesis and cell fate in the developing mammalian nervous system

Cited by 38 publications

References 51 publications

Notch maintains Drosophila type II neuroblasts by suppressing the expression of the Fez transcription factor Earmuff

Notch maintains Drosophila type II neuroblasts by suppressing the expression of the Fez transcription factor Earmuff

Mutual regulation between Satb2 and Fezf2 promotes subcerebral projection neuron identity in the developing cerebral cortex

AIRE: a missing link to explain female susceptibility to autoimmune diseases

Contact Info

Product

Resources

About