<i>Hes</i>genes regulate size, shape and histogenesis of the nervous system by control of the timing of neural stem cell differentiation

Hatakeyama, Jun; Bessho, Yasumasa; Katoh, Kazuo; Ookawara, Shigeo; Fujioka, Makio; Guillemot, François; Kageyama, Ryoichiro

doi:10.1242/dev.01436

Cited by 540 publications

(489 citation statements)

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“…The negatively acting bHLH factors commonly consist of unique amino acid residues in the basic domain and in the C-terminal region (Sasai et al, 1992;Thomas et al, 1992). They act by directly repressing transcription of positively acting bHLH genes and/or antagonizing the activity of positively acting bHLH factors (Sasai et al, 1992;Thomas and Rathjen, 1992;Akazawa et al, 1995;Ishibashi et al, 1995;Jarriault et al, 1995;Tomita et al, 1996;Chen et al, 1997;Ohtsuka et al, 1999;Kageyama et al, 2000;Cau et al, 2000;Hatakeyama et al, 2004;Hu et al, 2004). Hes6 is structurally related to negatively acting bHLH factors and contains characteristic amino acid sequences of this class (Pissarra et al, 2000;Vasiliaudkas et al, 2000).…”

Section: Potential Role Of Hes6 In Inner Ear Developmentmentioning

confidence: 99%

“…In contrast to positive-acting bHLH genes such as Math1, Hes genes are transcriptional repressors (Sasai et al, 1992;Thomas and Rathjen, 1992;Akazawa et al, 1995;Ishibashi et al, 1995;Jarriault et al, 1995;Chen et al, 1997;Ohtsuka et al, 1999;Kageyama et al, 2000). They are capable of repressing directly the transcription of positively acting bHLH genes and inhibiting the positively acting bHLH heterodimers from binding to their DNA targets (Akazawa et al, 1995;Ishibashi et al, 1995;Tomita et al, 1996;Ohtsuka et al, 1999;Cau et al, 2000;Hatakeyama et al, 2004;Hu et al, 2004). Therefore, Hes genes commonly exhibit an anti-neurogenic effect and, therefore, are considered to be negatively acting bHLH genes.…”

Section: Introductionmentioning

confidence: 99%

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Basic helix–loop–helix gene Hes6 delineates the sensory hair cell lineage in the inner ear

et al. 2006

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The basic helix-loop-helix (bHLH) gene Hes6 is known to promote neural differentiation in vitro. Here, we report the expression and functional studies of Hes6 in the inner ear. The expression of Hes6 appears to be parallel to that of Math1 (also known as Atoh1), a bHLH gene necessary and sufficient for hair cell differentiation. Hes6 is expressed initially in the presumptive hair cell precursors in the cochlea. Subsequently, the expression of Hes6 is restricted to morphologically differentiated hair cells. Similarly, the expression of Hes6 in the vestibule is in the hair cell lineage. Hes6 is dispensable for hair cell differentiation, and its expression in inner ear hair cells is abolished in the Math1-null animals. Furthermore, the introduction of Hes6 into the cochlea in vitro is not sufficient to promote sensory or neuronal differentiation. Therefore, Hes6 is downstream of Math1 and its expression in the inner ear delineates the sensory lineage. However, the role of Hes6 in the inner ear remains elusive.

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Section: Potential Role Of Hes6 In Inner Ear Developmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Basic helix–loop–helix gene Hes6 delineates the sensory hair cell lineage in the inner ear

et al. 2006

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“…Hes1, Hes3, and Hes5 suppress neuronal differentiation by repressing expression of, amongst other targets, Ngn1 and Ngn2 via activation of Math1 (Atoh1) (Kriks et al, 2005). As downregulation of Hes1, Hes3, and Hes5 leads to premature neuronal differentiation (Hatakeyama et al, 2004;Wong et al, 2008) and their decrease would lead to upregulation of Ngn1 and Ngn2, which in turn would lead to an increase in neurogenesis (Leucht et al, 2008).…”

Section: Dll1mentioning

confidence: 99%

“…However, these mouse models often die in utero or shortly after birth and, additionally, few mutant models of caudal closed NTDs exist (Bell et al, 2003;Bulgakov et al, 2004;Finnell et al, 2002;Friedman and Kaester, 2006;Hatakeyama et al, 2004;Hirata et al, 2001;Nagai et al, 2000;Pierani et al, 2001;Sahara et al, 2007;Tachibana et al, 2002;Xu et al, 1999). This is in sharp contrast to what is seen in humans in which spina bifida occulta (a caudal closed NTD) is the most common.…”

Section: Introductionmentioning

confidence: 99%

“…Examination of the cells present at the site of the lesions shows that NTDs are due to a wide range of reasons: increased/ decreased apoptosis, altered cellular proliferation, and premature differentiation into neural cells (Copp et al, 2003 includes an online table that is comprehensive in listing mouse models of NTDs and the believed or known primary cause; Hatakeyama et al, 2004;Hirata et al, 2001;Keller-Peck and Mullen, 1997;Wong et al, 2008;Xu et al, 1999;Yang et al, 2006). It is unknown if human NTDs share a similar range in diverse etiology, which makes pinpointing of all the contributing factors difficult.…”

Section: Introductionmentioning

confidence: 99%

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A new perspective on neural tube defects: Folic acid and microRNA misexpression

Shookhoff

Gallicano

2010

Genesis

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Summary: Neural tube defects (NTDs) are the second most common birth defects in the United States. It is well known that folic acid supplementation decreases about 70% of all NTDs, although the mechanism by which this occurs is still relatively unknown. The current theory is that folic acid deficiency ultimately leads to depletion of the methyl pool, leaving critical genes unmethylated, and, in turn, their improper expression leads to failure of normal neural tube development. Recently, new studies in human cell lines have shown that folic acid deficiency and DNA hypomethylation can lead to misexpression of microRNAs (miRNAs). Misexpression of critical miRNAs during neural development may lead to a subtle effect on neural gene regulation, causing the sometimes mild to severely debilitating range of phenotypes exhibited in NTDs. This review seeks to cohesively integrate current information regarding folic acid deficiency, methylation cycles, neural development, and miRNAs to propose a potential model of NTD formation. In addition, we have examined the relevant gene pathways and miRNAs that are predicted to affect them, and based on our investigation, we have devised a basic template of experiments for exploring the idea that miRNA misregulation may be linked to folic acid deficiency and NTDs. genesis 48:282-294, 2010. V V C 2010 Wiley-Liss, Inc.

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Coupling progenitor and neuronal diversity in the developing neocortex

Govindan

Jabaudon

2017

FEBS Letters

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The adult neocortex is composed of several types of glutamatergic neurons, which are sequentially born from progenitors during development. The extent and nature of progenitor diversity, and how it relates to neuronal diversity, is still poorly understood. In this review, we discuss key features of neocortical progenitors across several species, including their morphological properties, cell cycling behaviour and molecular signatures, and how these features relate to the competence of these cells to generate distinct types of progenies. Keywords: neocortical development; neurogenesis; progenitor diversityThe adult neocortex is composed of several types of glutamatergic neurons, which assemble during development to form the circuits underlying many of our conscious perceptions and motor actions. These distinct neuronal subtypes are sequentially born from progenitors, but the extent and nature of progenitor diversity, and how it relates to neuronal diversity, is still poorly understood.Neocortical neurons are generated by progenitors located in the ventricular zone (VZ), which is located below the cortical plate (i.e. developing cortex) and lines the walls of the ventricles [1]. In mice, neurogenesis starts on the tenth embryonic day (E10.5) and proceeds for about a week, until E18.5, after which astrogliogenesis occurs (see Ref.[2] for a recent review). Early born neurons migrate to form the deepest cortical layers (layers 6 and 5) while later born neurons migrate past them to reside more superficially and form upper layers (layer 2, 3 and 4). Deep layer neurons mostly send their axons to subcortical targets such as the thalamus, hindbrain or spinal cord, while superficial layer neurons mostly project intracortically, either locally (layer 4 neurons), or by forming longrange intracortical and interhemispheric projections.

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Hesgenes regulate size, shape and histogenesis of the nervous system by control of the timing of neural stem cell differentiation

Abstract: SummaryHes genes regulate size, shape and histogenesis of the nervous system by control of the timing of neural stem cell differentiation

Cited by 540 publications

References 61 publications

Basic helix–loop–helix gene Hes6 delineates the sensory hair cell lineage in the inner ear

Basic helix–loop–helix gene Hes6 delineates the sensory hair cell lineage in the inner ear

A new perspective on neural tube defects: Folic acid and microRNA misexpression

Coupling progenitor and neuronal diversity in the developing neocortex

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