Vertebrate Hox gene regulation: clustering and/or colinearity?

Duboule, Denis

doi:10.1016/s0959-437x(98)80004-x

Cited by 143 publications

(79 citation statements)

References 23 publications

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“…8A) and rendering enhancer sharing between both genes unlikely . This is in contrast to the transcriptional regulation of the well-studied Irx and Hox developmental gene clusters, in which enhancer sharing occurs extensively, possibly underlying the conservation of their genomic organization during evolution (Duboule, 1998;Tena et al, 2011). Hi-C in human cells, probing contact profiles at a genome-wide level, confirmed that the separated domain organization of the TBX3-TBX5 locus is conserved between mouse and human (Jin et al, 2013).…”

Section: Genomic Variation Affects Ccs Functionmentioning

confidence: 85%

The formation and function of the cardiac conduction system

2016

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The cardiac conduction system (CCS) consists of distinctive components that initiate and conduct the electrical impulse required for the coordinated contraction of the cardiac chambers. CCS development involves complex regulatory networks that act in stage-, tissue-and dose-dependent manners, and recent findings indicate that the activity of these networks is sensitive to common genetic variants associated with cardiac arrhythmias. Here, we review how these findings have provided novel insights into the regulatory mechanisms and transcriptional networks underlying CCS formation and function.

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Section: Genomic Variation Affects Ccs Functionmentioning

confidence: 85%

The formation and function of the cardiac conduction system

2016

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“…Homeotic (Hox) gene complexes are arranged in the same order in the genome as the domain where they function along the antero-posterior axis (Lewis, 1978;Harding et al, 1985;Duboule, 1998). In contrast, genes in the human β-globin cluster are lined in the order of temporal timing of expression (Jane and Cunningham, 1996;Li et al, 2006).…”

Section: Coordination Of Regulationmentioning

confidence: 99%

Developmental expression patterns of cuticular protein genes with the R&R Consensus from Anopheles gambiae

Togawa

Dunn

Emmons

et al. 2008

Insect Biochemistry and Molecular Biology

106

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CPR proteins are the largest cuticular protein family in arthropods. The whole genome sequence of Anopheles gambiae revealed 156 genes that code for proteins with the R&R Consensus and named CPRs. This protein family can be divided into RR-1 and RR-2 subgroups, postulated to contribute to different regions of the cuticle. We determined the temporal expression patterns of these genes throughout post-embryonic development by means of real-time qRT-PCR. Based on expression profiles, these genes were grouped into 21 clusters. Most of the genes were expressed with sharp peaks at single or multiple periods associated with molting. Genes coding for RR-1 and RR-2 proteins were found together in several co-expression clusters. Twenty-five genes were expressed exclusively at one metamorphic stage. Five out of six X-linked genes showed equal expression in males and females, supporting the presence of a gene dosage compensation system in An. gambiae. Many RR-2 genes are organized into sequence clusters whose members are extremely similar to each other and generally closely associated on a chromosome. Most genes in each sequence cluster are expressed with the same temporal expression pattern and at the same level, suggesting a shared mechanism to regulate their expression.

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“…The 39 murine Hox genes encode transcription factors possessing a conserved 60 amino acid DNA-binding motif, the homeodomain (Gehring, 1993;Phelan et al, 1995). Mammalian Hox genes are distributed in four clusters, Hoxa-Hoxd, on separate chromosomes and have been proposed to have evolved by duplication of an ancestral complex related to the HOM-C genes of Drosophila (Duboule and Dollé, 1989;Duboule, 1998;Ferrier and Holland, 2001). In the mouse, Hox gene expression is initiated at embryonic day (E)7.5 in the primitive streak, with expression subsequently expanding anteriorly in the neural tube and mesoderm until a predetermined rostral limit is reached (Deschamps and Wijgerde, 1993;Oosterveen et al, 2003;Roelen et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Retinoic acid regulates a subset of Cdx1 function in vivo

2003

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mechanism or through an intermediary; these mechanisms are not necessarily exclusive. In this regard, we have found that Cdx1 may serve as such an intermediary. Cdx1 encodes a homeobox transcription factor that is crucial for normal somitic expression of several Hox genes, and is regulated by retinoid signalling in vivo and in vitro likely through an atypical RARE in the proximal promoter. In order to more fully understand the relationship between retinoid signalling, Cdx1 expression and AP patterning, we have derived mice in which the RARE has been functionally inactivated. These RARE-null mutants exhibit reduced expression of Cdx1 at all stages examined, vertebral homeotic transformations and altered Hox gene expression which correlates with certain of the defects seen in Cdx1-null offspring. These findings are consistent with a pivotal role for retinoid signalling in governing a subset of expression of Cdx1 crucial for normal vertebral patterning. Research article 6556 retinoic acid (RA) plays a crucial role (Marshall et al., 1996). RA can induce Hox genes in embryocarcinoma cells in a manner reminiscent of the normal temporal activation of Hox expression, with 3′ genes from a given cluster responding earlier, and to lower concentrations of RA, than more 5′ members (Boncinelli et al., 1991;Simeone et al., 1990). In vivo, administration of exogenous RA to mouse embryos between E7.5 and E8.5 typically results in anteriorization of a number of Hox genes in a manner that correlates with posterior vertebral homeotic transformations (Conlon and Rossant, 1992;Kessel, 1992;Kessel and Gruss, 1991). Similar effects are also elicited by RA on expression of Hox genes in the CNS and concomitant perturbation of rhombomere patterning (Gavalas and Krumlauf, 2000;Gould et al., 1998;Marshall et al., 1992).The RA signal is transduced by the RA receptors (RARα, RARβ, RARγ and their isoforms). RARs belong to the family of ligand-inducible nuclear receptors and regulate expression of retinoid target genes as heterodimers with a retinoid X receptor (RXRα, RXRβ, RXRγ) partner. RXR-RAR heterodimers function by binding to cis-acting regulatory sequences (RAREs) present in the promoter region of target genes (Chambon, 1996;Mangelsdorf et al., 1995). Consensus RAREs have been described which consist of direct repeats (DR) of the sequence PuG(G/T)TCA with two or five nucleotides intervening the repeats (a DR2 or a DR5 element, respectively). RAREs are, however, highly polymorphic, and a number of variant motifs have been described (Huang et al., 2002;Glass, 1996). Retinoid signaling is also tightly controlled by the opposing actions of RALDH2, which is essential for the generation of most embryonic RA, and CYP26 members, which catabolizes RA (Swindell et al., 1999;Sakai et al., 2001; Abu-Abed et al., 1998;MacLean et al., 2001;Perlmann, 2002).A role for endogenous retinoid signaling in affecting Hox expression and AP patterning is supported by numerous studies (Gavalas et al., 1998;Huang et al., 1998;Zhang et al., 1997). Vertebral homeos...

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Vertebrate Hox gene regulation: clustering and/or colinearity?

Cited by 143 publications

References 23 publications

The formation and function of the cardiac conduction system

The formation and function of the cardiac conduction system

Developmental expression patterns of cuticular protein genes with the R&R Consensus from Anopheles gambiae

Retinoic acid regulates a subset of Cdx1 function in vivo

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