Tissue specific regulation of the chick Sox10E1 enhancer by different Sox family members

Murko, Christina; Bronner‐Fraser, Marianne

doi:10.1016/j.ydbio.2016.12.004

Cited by 12 publications

(13 citation statements)

References 33 publications

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“…Different enhancers control the activity of neural crest specifier genes Foxd3 and Sox10 in the cranial neural crest versus the trunk neural crest [29,45,59]. For instance, two enhancers for Foxd3 , NC1 and NC2, are activated differentially in the cranial and trunk crest, respectively.…”

Section: Neural Crest Formation Along the Body Axismentioning

confidence: 99%

“…The chick cranial specific enhancer, 10E2 , is regulated by neural crest specifiers Myb, Ets1, Sox9 [45]. In the trunk, Sox5 and Sox8 directly interact with the trunk specific enhancer, 10E1 [59]. Enhancer analysis in the mouse revealed seven enhancer regions that were directly bound by Pax3/7, Tfap2a, FoxD3, TCF/Lef, Sox10, as well as other Sox proteins [60,61].…”

Section: Transcriptional Control Of Morphogenesismentioning

confidence: 99%

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Regulatory Logic Underlying Diversification of the Neural Crest

2017

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The neural crest is a transient, multipotent population of cells that arises at the border of the developing nervous system. After closure of the neural tube, these cells undergo an epithelial to mesenchymal transition to delaminate and migrate, often to distinct locations in the embryo. Neural crest cells give rise to a diverse array of derivatives including neurons and glia of the peripheral nervous system, melanocytes, and bone and cartilage of the face. A gene regulatory network (GRN) controls specification, delamination, migration, and differentiation of this fascinating cell type. With increasing technological advances, direct linkages within the neural crest GRN are being uncovered. The underlying circuitry is useful for understanding important topics such as reprogramming, evolution, and disease.

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Section: Neural Crest Formation Along the Body Axismentioning

confidence: 99%

Section: Transcriptional Control Of Morphogenesismentioning

confidence: 99%

Regulatory Logic Underlying Diversification of the Neural Crest

2017

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“…Gain-of-function cis-regulatory changes, such as the appearance of new transcription factor binding sites, likely facilitated co-option of preexisting gene batteries, including the pro-chondrocytic SoxE genes and other mesenchymal gene programs, into neural crest-like cells at the neural plate border 2 . Indeed, we show that the lamprey SoxE1 enhancer harbours conserved binding site motifs for several important neural crest transcription factors, including Tfap and SoxE factors, which are known to activate and maintain SoxE transcription in the chick 56,57 , zebrafish 58 and lamprey 29 . HoxA2/B3 sites are also present and possibly control the activity pattern of the enhancer confined to specific regions of cranial neural crest conserved across vertebrate taxa 43 .…”

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confidence: 91%

A genome-wide assessment of the ancestral neural crest gene regulatory network

Hockman

Chong

Gavriouchkina

et al. 2018

Preprint

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The neural crest is an embryonic cell population that contributes to key vertebrate-specific features including the craniofacial skeleton and peripheral nervous system. Here we examine the transcriptional profiles and chromatin accessibility of neural crest cells in the basal sea lamprey, in order to gain insight into the ancestral state of the neural crest gene regulatory network (GRN) at the dawn of vertebrates. Transcriptome analyses reveal clusters of co-regulated genes during neural crest specification and migration that show high conservation across vertebrates for dynamic programmes like Wnt modulation during the epithelial to mesenchymal transition, but also reveal novel transcription factors and cell-adhesion molecules not previously implicated in neural crest migration. ATAC-seq analysis refines the location of known cis-regulatory elements at the Hox-α2 locus and uncovers novel cis-regulatory elements for Tfap2B and SoxE1. Moreover, cross-species deployment of lamprey elements in zebrafish reveals that the lamprey SoxE1 enhancer activity is deeply conserved, mediating homologous expression in jawed vertebrates. Together, our data provide new insight into the core elements of the GRN that are conserved to the base of the vertebrates, as well as expose elements that are unique to lampreys.

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“…(a) The sequences for Sall4 and SoxE binding in the core sequence. (b) Ch IP ‐ qPCR analysis demonstrating the binding of Sall4 (a), Sox8 (b) and Sox9 (c) to Otic1 sequence, in comparison with no‐binding control sequences in chromosome four gene desert region (Chr4 GD ) (Murko & Bronner, ) and ovalbumin intron 1 sequence (Sugahara et al., ). Ch IP ‐ qPCR with each of the antibodies and normal rabbit IgG was performed using four biological replicates for each genomic site.…”

Section: Resultsmentioning

confidence: 99%

“…This led to Pax2-positive cell patches representing the otic placode tissue developing in a way that was dependent on the addition of Fgf factor in the second phase of the culture (Figure 7c). (Murko & Bronner, 2017) and ovalbumin intron 1 sequence (Sugahara et al, 2018). ChIP-qPCR with each of the antibodies and normal rabbit IgG was performed using four biological replicates for each genomic site.…”

Section: Otic1 Activity In Otic Placode Tissue Developed From Mousementioning

confidence: 99%

Cooperation of Sall4 and Sox8 transcription factors in the regulation of the chicken Sox3 gene during otic placode development

et al. 2018

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To elucidate the transcriptional regulation that underlies specification of the otic placode, we investigated the Sox3 downstream enhancer Otic1 of the chicken, the activity of which is restricted to and distributed across the entire otic placode. The 181-bp Otic1 enhancer sequence was dissected into a 68-bp minimal activating sequence, which exhibited dimer enhancer activity in the otic placode and cephalic neural crest, and this was further reduced to a 25-bp Otic1 core sequence, which also showed octamer enhancer activity in the same regions. The Otic1 core octamer was activated by the combined action of Sall4 and the SoxE transcription factors (TFs) Sox8 or Sox9. Binding of Sall4, Sox8 and Sox9 to the Otic1 sequence in embryonic tissues was confirmed by ChIP-qPCR analysis. The core-adjoining 3' side sequences of Otic1 augmented its enhancer activity, while inclusion of the CAGGTG sequence in the immediate 3' end of the 68-bp sequence repressed its enhancer activity outside the otic placode. The CAGGTG sequence likely serves as the binding sites of the repressor TFs δEF1 (Zeb1), Sip1 (Zeb2), and Snail2, all of which are expressed in the cephalic neural crest but not in the otic placode. Therefore, the combination of Sall4-Sox8-dependent activation and CAGGTG sequence-dependent repression determines otic placode development. Although the Otic1 sequence is not conserved in mammals or fishes, the activation mechanism is, as Otic1 was also activated in otic placode tissues developed from mouse embryonic stem cells and transient transgenic zebrafish embryos.

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Tissue specific regulation of the chick Sox10E1 enhancer by different Sox family members

Cited by 12 publications

References 33 publications

Regulatory Logic Underlying Diversification of the Neural Crest

Regulatory Logic Underlying Diversification of the Neural Crest

A genome-wide assessment of the ancestral neural crest gene regulatory network

Cooperation of Sall4 and Sox8 transcription factors in the regulation of the chicken Sox3 gene during otic placode development

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