Six2 functions redundantly immediately downstream of Hoxa2

Kutějová, Eva; Engist, Bettina; Self, Michelle; Oliver, Guillermo; Kirilenko, Pavel; Bobola, Nicoletta

doi:10.1242/dev.017624

Cited by 44 publications

(51 citation statements)

References 42 publications

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“…This results in direct or indirect negative regulation of relevant transcription factors normally expressed in PA1 [including Pitx1 (paired-like homeodomain transcription factor 1), Lhx6 (LIM homeobox protein 6), Six2 (sine oculis-related homeobox 2 homologue), Alx4 (aristalesslike homeobox 4), Bapx1 (Nkx3-2 -Mouse Genome Informatics) and Barx1 (BraH-like homeobox 1)] (Fig. 3A) (Bobola et al, 2003;Kanzler et al, 1998;Kutejova et al, 2005;Kutejova et al, 2008;Minoux et al, 2009;Santagati et al, 2005).…”

Section: Trokovic Et Al 2003mentioning

confidence: 99%

Molecular mechanisms of cranial neural crest cell migration and patterning in craniofacial development

2010

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SummaryDuring vertebrate craniofacial development, neural crest cells (NCCs) contribute much of the cartilage, bone and connective tissue that make up the developing head. Although the initial patterns of NCC segmentation and migration are conserved between species, the variety of vertebrate facial morphologies that exist indicates that a complex interplay occurs between intrinsic genetic NCC programs and extrinsic environmental signals during morphogenesis. Here, we review recent work that has begun to shed light on the molecular mechanisms that govern the spatiotemporal patterning of NCC-derived skeletal structures -advances that are central to understanding craniofacial development and its evolution.

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Section: Trokovic Et Al 2003mentioning

confidence: 99%

Molecular mechanisms of cranial neural crest cell migration and patterning in craniofacial development

2010

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“…Although CCs are non-essential to the worm under standard laboratory conditions (Fares and Greenwald, 2001a), they have been recently shown to be important in heavy metal detoxification (Schwartz et al, 2010), a function performed by vertebrate kidneys. Intriguingly, the specification of CC fate requires CEH-34, a Six2 transcription factor whose mammalian homolog is the master regulator of kidney development in the intermediate mesoderm (Self et al, 2006;Kobayashi et al, 2008;Kutejova et al, 2008).…”

Section: Research Articlementioning

confidence: 99%

The FoxF/FoxC factor LET-381 directly regulates both cell fate specification and cell differentiation inC. elegansmesoderm development

Amin

Shi

2010

Development

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SUMMARYForkhead transcription factors play crucial and diverse roles in mesoderm development. In particular, FoxF and FoxC genes are, respectively, involved in the development of visceral/splanchnic mesoderm and non-visceral mesoderm in coelomate animals. Here, we show at single-cell resolution that, in the pseudocoelomate nematode C. elegans, the single FoxF/FoxC transcription factor LET-381 functions in a feed-forward mechanism in the specification and differentiation of the non-muscle mesodermal cells, the coelomocytes (CCs). LET-381/FoxF directly activates the CC specification factor, the Six2 homeodomain protein CEH-34, and functions cooperatively with CEH-34/Six2 to directly activate genes required for CC differentiation. Our results unify a diverse set of studies on the functions of FoxF/FoxC factors and provide a model for how FoxF/FoxC factors function during mesoderm development.

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“…Pou6f2 was used as a positive control and Itih4 as a negative control (Donaldson et al, 2012). The Hoxa2 antibody used for ChIP was described previously (Kutejova et al, 2008).…”

Section: Chromatin Immunoprecipitationmentioning

confidence: 99%

A distal 594bp ECR specifies Hmx1 expression in pinna and lateral facial morphogenesis and is regulated by Hox-Pbx-Meis

Rosin

Cox

et al. 2016

Development

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Hmx1 encodes a homeodomain transcription factor expressed in the developing lateral craniofacial mesenchyme, retina and sensory ganglia. Mutation or mis-regulation of Hmx1 underlies malformations of the eye and external ear in multiple species. Deletion or insertional duplication of an evolutionarily conserved region (ECR) downstream of Hmx1 has recently been described in rat and cow, respectively. Here, we demonstrate that the impact of Hmx1 loss is greater than previously appreciated, with a variety of lateral cranioskeletal defects, auriculofacial nerve deficits, and duplication of the caudal region of the external ear. Using a transgenic approach, we demonstrate that a 594 bp sequence encompassing the ECR recapitulates specific aspects of the endogenous Hmx1 lateral facial expression pattern. Moreover, we show that Hoxa2, Meis and Pbx proteins act cooperatively on the ECR, via a core 32 bp sequence, to regulate Hmx1 expression. These studies highlight the conserved role for Hmx1 in BA2-derived tissues and provide an entry point for improved understanding of the causes of the frequent lateral facial birth defects in humans.

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Six2 functions redundantly immediately downstream of Hoxa2

Cited by 44 publications

References 42 publications

Molecular mechanisms of cranial neural crest cell migration and patterning in craniofacial development

Molecular mechanisms of cranial neural crest cell migration and patterning in craniofacial development

The FoxF/FoxC factor LET-381 directly regulates both cell fate specification and cell differentiation inC. elegansmesoderm development

A distal 594bp ECR specifies Hmx1 expression in pinna and lateral facial morphogenesis and is regulated by Hox-Pbx-Meis

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