Early B-cell factors 2 and 3 (EBF2/3) regulate early migration of Cajal–Retzius cells from the cortical hem

Chiara, Francesca; Badaloni, Aurora; Croci, Laura; Yeh, Mason L.; Cariboni, Anna; Hoerder‐Suabedissen, Anna; Consalez, G. Giacomo; Eickholt, Britta J.; Shimogori, Tomomi; Parnavelas, John G.; Rakić, Sonja

doi:10.1016/j.ydbio.2012.02.034

Cited by 43 publications

(65 citation statements)

References 59 publications

(58 reference statements)

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“…In Arx (GCG)7 mice, ectopic Ebf3 expression in developing interneurons disrupted their migration, whereas Lmo1 and Shox2 remained repressed (42). Normally, Ebf1/2/3 genes appear to control embryonic migration of Cajal-Retzius cells (57). Lgi1 is a secreted protein expressed by central nervous system neurons that participates in synapse organization and neuronal growth (58, 59), and loss-of-function mutations are associated with temporal lobe epilepsy in human patients (60).…”

Section: Discussionmentioning

confidence: 99%

Neonatal Estradiol Stimulation Prevents Epilepsy in Arx Model of X-Linked Infantile Spasms Syndrome

2014

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Infantile spasms are a catastrophic form of pediatric epilepsy with inadequate treatment. In patients, mutation of ARX, a transcription factor selectively expressed in neuronal precursors and adult inhibitory interneurons, impairs cell migration and causes a major inherited subtype of the disease X-linked infantile spasms syndrome. Using an animal model, the Arx(GCG)10+7 mouse, we determined that brief estradiol (E2) administration during early postnatal development prevented spasms in infancy and seizures in adult mutants. E2 was ineffective when delivered after puberty or 30 days after birth. Early E2 treatment altered mRNA levels of three downstream targets of Arx (Shox2, Ebf3, and Lgi1) and restored depleted interneuron populations without increasing GABAergic synaptic density. Postnatal E2 treatment may induce lasting transcriptional changes that lead to enduring disease modification and could potentially serve as a therapy for inherited interneuronopathies.

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Section: Discussionmentioning

confidence: 99%

Neonatal Estradiol Stimulation Prevents Epilepsy in Arx Model of X-Linked Infantile Spasms Syndrome

2014

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“…Consistent with previous reports that Foxg1 can act as a transcriptional repressor (Yao et al, 2001), we observed an increased representation of TFs among the down-regulated genes (Figure 4) and showed that Foxg1 binds to these down-regulated genes in vivo (Figure 5). Interestingly, these TFs might not only be selectively expressed, but may also be required for CR cell development (Chiara et al, 2012; Inoue et al, 2008). These results indicate that the transition from early CR cell to the projection neuron production program involves the rapid repression of multiple TFs (≥20 hr), followed by delayed induction of up-regulated TFs (≥30 hr).…”

Section: Discussionmentioning

confidence: 99%

Foxg1 Coordinates the Switch from Nonradially to Radially Migrating Glutamatergic Subtypes in the Neocortex through Spatiotemporal Repression

Kumamoto¹,

Toma²,

Gunadi³

et al. 2013

Cell Reports

108

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SUMMARY The specification of neuronal subtypes in the cerebral cortex proceeds in a temporal manner; however, the regulation of the transitions between the sequentially generated subtypes is poorly understood. Here, we report that the forkhead-box transcription factor Foxg1 coordinates the production of neocortical projection neurons through the global repression of a default gene program. The delayed activation of Foxg1 was necessary and sufficient to induce deep-layer neurogenesis, followed by a sequential wave of upper-layer neurogenesis. A genome-wide analysis revealed that Foxg1 binds to mammalian-specific non-coding sequences to repress over 12 transcription factors expressed in early progenitors, including Ebf2/3, Dmrt3, Dmrta1 and Eya2. These findings reveal an unexpected prolonged competence of progenitors to initiate corticogenesis at a progressed stage during development and identify Foxg1 as a critical initiator of neocorticogenesis through spatiotemporal repression, a system that balances the production of non-radially and radially migrating glutamatergic subtypes during mammalian cortical expansion.

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“…A transactivation domain (TAD) at the C terminus mediates activation of Ebf target genes 13,14 . As all four proteins share over 90% sequence homology within these domains, except for the TAD, all Ebf proteins bind to the same DNA sequence and can act redundantly [15][16][17] .…”

mentioning

confidence: 99%

“…Originally identified in neuronal cells 18,19 , Ebf3 is important for cell migration in the developing cortex 17 and in the projection of olfactory neurons to the olfactory bulb 16 . In Xenopus the homologue Xebf3 acts as a regulator of neuronal differentiation downstream of XNeuroD 20 .…”

mentioning

confidence: 99%

Ebf factors and MyoD cooperate to regulate muscle relaxation via Atp2a1

et al. 2014

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Myogenic regulatory factors such as MyoD and Myf5 lie at the core of vertebrate muscle differentiation. However, E-boxes, the cognate binding sites for these transcription factors, are not restricted to the promoters/enhancers of muscle cell-specific genes. Thus, the specificity in myogenic transcription is poorly defined. Here we describe the transcription factor Ebf3 as a new determinant of muscle cell-specific transcription. In the absence of Ebf3 the lung does not unfold at birth, resulting in respiratory failure and perinatal death. This is due to a hypercontractile diaphragm with impaired Ca 2 þ efflux-related muscle functions. Expression of the Ca 2 þ pump Serca1 (Atp2a1) is downregulated in the absence of Ebf3, and its transgenic expression rescues this phenotype. Ebf3 binds directly to the promoter of Atp2a1 and synergises with MyoD in the induction of Atp2a1. In skeletal muscle, the homologous family member Ebf1 is strongly expressed and together with MyoD induces Atp2a1. Thus, Ebf3 is a new regulator of terminal muscle differentiation in the diaphragm, and Ebf factors cooperate with MyoD in the induction of muscle-specific genes.

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Early B-cell factors 2 and 3 (EBF2/3) regulate early migration of Cajal–Retzius cells from the cortical hem

Cited by 43 publications

References 59 publications

Neonatal Estradiol Stimulation Prevents Epilepsy in Arx Model of X-Linked Infantile Spasms Syndrome

Neonatal Estradiol Stimulation Prevents Epilepsy in Arx Model of X-Linked Infantile Spasms Syndrome

Foxg1 Coordinates the Switch from Nonradially to Radially Migrating Glutamatergic Subtypes in the Neocortex through Spatiotemporal Repression

Ebf factors and MyoD cooperate to regulate muscle relaxation via Atp2a1

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