Directed Migration of Cortical Interneurons Depends on the Cell-Autonomous Action of Sip1

Berghe, Veronique van den; Stappers, Elke; Vandesande, Bram; Dimidschstein, Jordane; Kroes, Roel; Francis, Annick; Conidi, Andrea; Lesage, Flore; Dries, Ruben; Cazzola, Silvia; Berx, Geert; Kessaris, Nicoletta; Vanderhaeghen, Pierre; IJcken, Wilfred F. J. van; Grosveld, Frank; Goossens, Steven; Haigh, Jody J.; Fishell, Gord; Goffinet, André M.; Aerts, Stein; Huylebroeck, Danny; Seuntjens, Eve

doi:10.1016/j.neuron.2012.11.009

Cited by 121 publications

(124 citation statements)

References 64 publications

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“…In support of these findings, a similar study reported reduced cortical GABAergic interneurons, downregulation of cortical interneuron markers (including cMaf and Cxcr7) and increased Nkx2.1 expression, in mice with conditional knockout of Zeb2 in the MGE . The study by van den Berghe et al (2013) demonstrated that Zeb2 directly regulates the cortical migration of MGE-derived GABAergic interneurons, which express high levels of Zeb2. Zeb2 was shown to act cell-autonomously to direct cortical interneuronal migration through regulation of the precise levels of the Unc5b netrin-repulsive receptor, with Unc5b knockout also being shown to rescue the migration defect of the Zeb2 mutant mice .…”

Section: Zeb2 In Cerebral Developmentmentioning

confidence: 99%

Zeb2: A multifunctional regulator of nervous system development

Hegarty

Sullivan

O’Keeffe

2015

Progress in Neurobiology

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Section: Zeb2 In Cerebral Developmentmentioning

confidence: 99%

Zeb2: A multifunctional regulator of nervous system development

Hegarty

Sullivan

O’Keeffe

2015

Progress in Neurobiology

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“…We have read with interest the latest advances regarding ZEB2 gene function in neuroembryology and its connections with epilepsy (McKinsey et al, 2013;Van den Berghe et al, 2013). Zinc finger E-box binding homeobox 2 (ZEB2, MIM#60580), also annotated as ZFHX1B and SIP1, is a member of the two-handed zinc finger/homeodomain transcription factors.…”

Section: To the Editorsmentioning

confidence: 99%

Epilepsy in Mowat‐Wilson syndrome: Is it a matter of GABA?

et al. 2013

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“…45,46 Melanin content determination. Melanin was extracted with an alkaline solution as previously described.…”

mentioning

confidence: 99%

Identification of a ZEB2-MITF-ZEB1 transcriptional network that controls melanogenesis and melanoma progression

et al. 2014

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Deregulation of signaling pathways that control differentiation, expansion and migration of neural crest-derived melanoblasts during normal development contributes also to melanoma progression and metastasis. Although several epithelial-tomesenchymal (EMT) transcription factors, such as zinc finger E-box binding protein 1 (ZEB1) and ZEB2, have been implicated in neural crest cell biology, little is known about their role in melanocyte homeostasis and melanoma. Here we show that mice lacking Zeb2 in the melanocyte lineage exhibit a melanoblast migration defect and, unexpectedly, a severe melanocyte differentiation defect. Loss of Zeb2 in the melanocyte lineage results in a downregulation of the Microphthalmia-associated transcription factor (Mitf) and melanocyte differentiation markers concomitant with an upregulation of Zeb1. We identify a transcriptional signaling network in which the EMT transcription factor ZEB2 regulates MITF levels to control melanocyte differentiation. Moreover, our data are also relevant for human melanomagenesis as loss of ZEB2 expression is associated with reduced patient survival. Melanocytes are specialized cells in the skin that produce melanin, a pigment that is responsible for skin and hair color and that provides protection against ultraviolet (UV) radiation. During mouse embryogenesis, melanoblasts originate from the neural crest and migrate along a dorsolateral pathway from the neural tube to the developing dermis.1 Around embryonic day (E) E11 they move into the epidermis and eventually populate the developing hair follicle.2 Here they separate into two distinct populations: the differentiated pigmented melanocytes, which reside in the hair matrix, and the non-pigmented melanocyte stem cells (MSC) in the bulge. The latter cells are responsible for replenishing the hair follicle with new melanocytes during each hair cycle. Genetic studies in mice demonstrated the importance of several key players (such as sex-determining region Y (SRY)-box 10 (Sox10), paired-box 3 (Pax3), microphthalmia-associated transcription factor (Mitf), endothelin 3/endothelin receptor B (Edn3/ Ednrb), Kitl/Kit, Slug, cellular myelocytomatosis oncogene cellular homolog (cMyc) and b-Catenin (b-Cat)) for melanoblast cell fate specification, proliferation, migration and survival.2-4 The master regulator of the melanocyte development is MITF, which is spatio-temporally controlled by several key transcription factors such as SOX10, PAX3 and b-catenin.5-7 Fundamentally, MITF induces gene expression patterns that prompt a melanocyte to differentiate and initiate pigment production by activating genes important for melanin biosynthesis (such as Tyrosinase (Tyr), Dopachrome tautomerase (Dct), Tyrosinase-related protein 1 (Tyrp1) and

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Directed Migration of Cortical Interneurons Depends on the Cell-Autonomous Action of Sip1

Cited by 121 publications

References 64 publications

Zeb2: A multifunctional regulator of nervous system development

Zeb2: A multifunctional regulator of nervous system development

Epilepsy in Mowat‐Wilson syndrome: Is it a matter of GABA?

Identification of a ZEB2-MITF-ZEB1 transcriptional network that controls melanogenesis and melanoma progression

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