The <i>Dlx5</i> and <i>Dlx6</i> homeobox genes are essential for craniofacial, axial, and appendicular skeletal development

Robledo, Raymond F.; Rajan, Lakshmi; Li, Xue; Lufkin, Thomas

doi:10.1101/gad.988402

Cited by 389 publications

(478 citation statements)

References 49 publications

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“…Deletion of the coding and intergenic regions of Dlx5 and Dlx6 with a single targeting event in the mouse results in perinatal death and in a limb malformation reminiscent of the human ectrodactyly, Split Hand Foot Malformation type I (Merlo et al, 2002;Robledo et al, 2002). In this study, we describe the craniofacial lesion present in Dlx5/6 double mutant mice.…”

Section: Introductionmentioning

confidence: 87%

Jaw transformation with gain of symmetry after Dlx5/Dlx6 inactivation: Mirror of the past?

Beverdam¹,

Merlo

Paleari³

et al. 2002

Genesis

179

225

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Section: Introductionmentioning

confidence: 87%

Jaw transformation with gain of symmetry after Dlx5/Dlx6 inactivation: Mirror of the past?

Beverdam¹,

Merlo

Paleari³

et al. 2002

Genesis

179

225

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“…In mice, Dlx transcription factors have been shown to have a key function in the development and morphogenesis of the limb skeleton. 3,12 Expression of Dlx5 and Dlx6 has been detected in the apical ectodermal ridge of the embryonic limb buds. Double knockout of Dlx5 and Dlx6 in the mouse leads to ectrodactyly.…”

Section: Review Of Literature and Discussionmentioning

confidence: 99%

Split hand/foot malformation due to chromosome 7q aberrations(SHFM1): additional support for functional haploinsufficiency as the causative mechanism

et al. 2009

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We report on three patients with split hand/foot malformation type 1 (SHFM1). We detected a deletion in two patients and an inversion in the third, all involving chromosome 7q21q22. We performed conventional chromosomal analysis, array comparative genomic hybridization and fluorescence in situ hybridization. Both deletions included the known genes associated with SHFM1 (DLX5, DLX6 and DSS1), whereas in the third patient one of the inversion break points was located just centromeric to these genes. These observations confirm that haploinsufficiency due to either a simultaneous deletion of these genes or combined downregulation of gene expression due to a disruption in the region between these genes and a control element could be the cause of the syndrome. We review previously reported studies that support this hypothetical mechanism.

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“…Expression analysis alone does not allow us to confirm or refute this hypothesis, but previous studies have confirmed the existence of redundant and distinct function in the morphogenesis of the skeleton by analysis of the Dlx1, Dlx2, Dlx1/Dlx2, Dlx5, Dlx2/Dlx5 and Dlx5/ Dlx6 mouse mutants (Qiu et al, 1995(Qiu et al, , 1997Acampora et al, 1999;Depew et al, 1999Depew et al, , 2005Robledo et al, 2002).…”

Section: Dermal Bonesmentioning

confidence: 97%

Expression of the dlx gene family during formation of the cranial bones in the zebrafish (Danio rerio): Differential involvement in the visceral skeleton and braincase

Verreijdt

Debiais-Thibaud

Borday-Birraux

et al. 2006

Developmental Dynamics

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We have used dlx genes to test the hypothesis of a separate developmental program for dermal and cartilage bones within the neuro-and splanchnocranium by comparing expression patterns of all eight dlx genes during cranial bone formation in zebrafish from 1 day postfertilization (dPF) to 15 dPF. dlx genes are expressed in the visceral skeleton but not during the formation of dermal or cartilage bones of the braincase. The spatiotemporal expression pattern of all the members of the dlx gene family, support the view that dlx genes impart cellular identity to the different arches, required to make arch-specific dermal bones. Expression patterns seemingly associated with cartilage (perichondral) bones of the arches, in contrast, are probably related to ongoing differentiation of the underlying cartilage rather than with differentiation of perichondral bones themselves. Whether dlx genes originally functioned in the visceral skeleton only, and whether their involvement in the formation of neurocranial bones (as in mammals) is secondary, awaits clarification. Developmental Dynamics 235:1371-1389, 2006.

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The Dlx5 and Dlx6 homeobox genes are essential for craniofacial, axial, and appendicular skeletal development

Cited by 389 publications

References 49 publications

Jaw transformation with gain of symmetry after Dlx5/Dlx6 inactivation: Mirror of the past?

Jaw transformation with gain of symmetry after Dlx5/Dlx6 inactivation: Mirror of the past?

Split hand/foot malformation due to chromosome 7q aberrations(SHFM1): additional support for functional haploinsufficiency as the causative mechanism

Expression of the dlx gene family during formation of the cranial bones in the zebrafish (Danio rerio): Differential involvement in the visceral skeleton and braincase

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