Ectopic expression of Hoxb-8 causes duplication of the ZPA in the forelimb and homeotic transformation of axial structures

Charité, Jeroen; Graaff, Wim de; Shen, Sanbing; Deschamps, Jacqueline

doi:10.1016/0092-8674(94)90524-x

Cited by 232 publications

(123 citation statements)

References 41 publications

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“…The latter function partly depends on RA-mediated induction of Hoxb8 in the forelimb but not the hindlimb (Lu et al, 1997;Stratford et al, 1997). Hoxb8 in turn activates Shh (Charite et al, 1994). This epistatic relation explains how exogenous RA may lead to Shh activation and formation of an ectopic ZPA.…”

Section: Retinoic Acidmentioning

confidence: 94%

“…Noticeably, Hoxd11 and Hoxd12 are not induced in this Hand2 mutant, suggesting that posterior Hoxd genes are required downstream of Hand2 to induce Shh. In addition, ectopic expression of Hoxb8 and Hoxd12 has unraveled the potential for Hox genes to induce Shh (Charite et al, 1994;Knezevic et al, 1997).…”

Section: Hoxd Genes and Early Posterior Restriction Of The Zpamentioning

confidence: 99%

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Anteroposterior patterning in the limb and digit specification: Contribution of mouse genetics

Robert

Lallemand

2006

Developmental Dynamics

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The limb has been a privileged object of investigation and reflection for scientists over the past two centuries and continues to provide a heuristic framework to analyze vertebrate development. Recently, accumulation of new data has significantly changed our view on the mechanisms of limb patterning, in particular along the anterior-posterior axis. These data have led us to revisit the mode of action of the zone of polarizing activity. They shed light on the molecular and cellular mechanisms of patterning linked to the Shh-Gli3 signaling pathway and give insights into the mechanism of activation of these cardinal factors, as well as the consequences of their activity. These new data are in good part the result of systematic Application of tools used in contemporary mouse molecular genetics. These have extended the power of mouse genetics by introducing mutational strategies that allow fine-tuned modulation of gene expression, interchromosomal deletions and duplication. They have even made the mouse embryo amenable to cell lineage analysis that used to be the realm of chick embryos. In this review, we focus on the data acquired over the last five years from the analysis of mouse limb development and discuss new perspectives opened by these results. Developmental Dynamics 235:2337-2352, 2006.

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Section: Retinoic Acidmentioning

confidence: 94%

Section: Hoxd Genes and Early Posterior Restriction Of The Zpamentioning

confidence: 99%

Anteroposterior patterning in the limb and digit specification: Contribution of mouse genetics

Robert

Lallemand

2006

Developmental Dynamics

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“…Hox genes has been established by their homology to Drosophila genes of known developmental significance (McGinnis and Krumlauf, 19921, by their suggestive embryonic expression patterns (Holland and Hogan, 1988), and by both dominant gain of function (Wolgemuth et al, 1989;Kessel et al, 1990;Kaur et al, 1992;McLain et al, 1992;Jegalian and De Robertis, 1992;Pollock et al, 1992;Lufkin et al, 1992;Charite et al, 1994) and recessive loss of function (Chisaka and Capecchi, 1991;Lufkin et al, 1991;Chisaka et al, 1992;Mouellic et al, 1992;Ramirez-Solis et al, 1993;Dolle et al, 1993;Small and Potter, 1993) mutational analyses in mice.…”

Section: Introductionmentioning

confidence: 99%

Gsh‐1: A novel murine homeobox gene expressed in the central nervous system

Valerius

Stock

et al. 1995

Developmental Dynamics

103

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We report the characterization of Gsh-1, a novel murine homeobox gene. Northern blot analysis revealed a transcript of approximately 2 kb in sue present at embryonic days 10.5, 11.5, and 12.5 of development. The cDNA sequence encoded a proline rich motif, a polyalanine tract, and a homeodomain with strong homology to those encoded by the clustered Hox genes. The Gsh-1 expression pattern was determined for days E8.5 to E13.5 by whole mount and serial section in situ hybridizations. Gsh-1 transcription was restricted to the central nervous system. Expression is present in the neural tube and hindbrain as two continuous, bilaterally symmetrical stripes within neural epithelial tissue. In the mesencephalon, expression is seen as a band across the most anterior portion. There is also diencephalon expression in the anlagen of the thalamus and the hypothalamus as well as in the optic stalk, optic recess, and the ganglionic eminence. Moreover, through the use of fusion proteins containing the Gsh-I homeodomain, we have determined the consensus DNA binding site of the Gsh-1 homeoprotein to be GCT/cA/,ATTAG/A. 0 1995 Wiley-Liss, Inc.

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“…In this way, a so-called Hox-code (Kessel and Gruss, 1991a) is imparted onto different regions of the developing skeleton, suggesting the involvement of individual Hox genes or specific Hox gene combinations in specifying unique regions. Indeed, elements of the skeleton develop abnormally when Hox genes are misexpressed in transgenic mice (Charite et al, 1994;Jegalian and DeRobertis, 1992;Kessel et al, 1990;Lufkin et al, 1992;Pollock et al, 1992). Similarly, the disruption of Hox genes by targeted mutagenesis leads to alterations in the skeleton (Boulet and Capecchi, 1996;Boulet and Capecchi, 2002;Capecchi, 1993, 1994;Capecchi, 1994, 1996;Davis et al, 1995;Favier et al, 1995;Favier et al, 1996;Fromental-Ramain et al, 1996a;Fromental-Ramain et al, 1996b;Horan et al, 1995a;Horan et al, 1994;Kostic and Capecchi, 1994;LeMouellic et al, 1989;RamirezSolis et al, 1993;Rancourt et al, 1995;Rijli et al, 1994;Rijli et al, 1993;Rijli et al, 1995;Saegusa et al, 1996;Small and Potter, 1995;Suemori et al, 1995.…”

Section: Regionalization Along the Anterior-posterior Axis: Hox Genesmentioning

confidence: 99%

“…This could be due to technical difficulties in distinguishing individual cervical and thoracic vertebrae. However, in Hox-transgenic mice, the alterations also most predominantly manifest at the cranial-cervical boundary (for Hoxb6: (Kaur et al, 1992); Hoxb7: (McLain et al, 1992); Hoxd4: (Lufkin et al, 1992), the cervico-thoracic boundary (for Hoxa4 and Hoxc8: (Sreenath et al, 1996); Hoxb8: (Charite et al, 1994), or the thoraciclumbar boundary (for Hoxc6: (Jegalian and DeRobertis, 1992); Hoxc8: (Pollock et al, 1992). Taken together, these lines of evidence may suggest that the transition regions may be more labile in their specification, or that their specification can be influenced within a larger time window.…”

Section: Regionalization Along the Anterior-posterior Axis: Hox Genesmentioning

confidence: 99%

Molecular basis for skeletal variation: insights from developmental genetic studies in mice

Kappen

Neubüser

Balling

et al. 2007

Birth Defects Research Pt B

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Skeletal variations are common in humans, and potentially are caused by genetic as well as environmental factors. We here review molecular principles in skeletal development to develop a knowledge base of possible alterations that could explain variations in skeletal element number, shape or size. Environmental agents that induce variations, such as teratogens, likely interact with the molecular pathways that regulate skeletal development. Birth Defects Res (Part B), 80:425–450, 2007. © 2007 Wiley‐Liss, Inc.

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Ectopic expression of Hoxb-8 causes duplication of the ZPA in the forelimb and homeotic transformation of axial structures

Cited by 232 publications

References 41 publications

Anteroposterior patterning in the limb and digit specification: Contribution of mouse genetics

Anteroposterior patterning in the limb and digit specification: Contribution of mouse genetics

Gsh‐1: A novel murine homeobox gene expressed in the central nervous system

Molecular basis for skeletal variation: insights from developmental genetic studies in mice

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