EVOLUTION OF <i>HOX</i> GENES

Ruddle, Frank H.; Bartels, Janet L.; Bentley, Kevin L.; Kappen, Claudia; Murtha, Michael T.; Pendleton, John W.

doi:10.1146/annurev.ge.28.120194.002231

Cited by 219 publications

(131 citation statements)

References 35 publications

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“…One family of human homeobox-containing genes is HOX whose prototype is HOM in Drosophila [4]. Thirty-nine HOX genes are clustered in a similar arrangement of 13 paralog groups on four different chromosomal/genomic regions, HOXA, B, C, and D and encode transcription factors [4][5][6][7]. They are expressed in a spatiotemporal manner during embryonic morphogenesis, each regulating a group of genes involved in modeling a specific segmental architecture.…”

Section: Introductionmentioning

confidence: 99%

HOXD3-overexpression increases integrin αvβ3 expression and deprives E-cadherin while it enhances cell motility in A549 cells

Ohta

Hamada

Tada

et al. 2006

Clin Exp Metastasis

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We have previously shown that transduction of HOXD3, one of homeobox genes, into human lung cancer A549 cells enhances cell motility, invasion and metastasis. In the present study, we examined the roles of integrin β3 which was up-regulated by HOXD3-overexpression in the HOXD3-induced motility of A549 cells. We first established integrin β3-transfectants and compared their motile activity to those of the HOXD3-transfected, control-transfected and parental cells by three different assays.The integrin β3-transfectants as well as the HOXD3-transfectants formed heterodimer with integrin αv subunit, and showed highly motile activities assessed by haptotaxis or phagokinetic track assay compared to the control transfectants or parental cells. In vitro wound-healing assay revealed that migratory activities were graded as the HOXD3-transfectants > the integrin β3-transfectants > the control transfectants or parental cells. E-cadherin was expressed in the integrin β3-transfectants but not expressed in the HOXD3-transfectants. An addition of function-blocking antibody to E-cadherin into the wound-healing assay promoted the migratory activity of the integrin β3-transfectants, suggesting that E-cadherin prevented the cells from dissociating from the wound edges. These results indicate that increased expression of integrin αv β3 and loss of E-cadherin by HOXD3-overexpression are responsible for the enhanced motility and dissociation.

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Section: Introductionmentioning

confidence: 99%

HOXD3-overexpression increases integrin αvβ3 expression and deprives E-cadherin while it enhances cell motility in A549 cells

Ohta

Hamada

Tada

et al. 2006

Clin Exp Metastasis

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“…They are involved in the development of vertebrate body plan characters [59] and are one of the best-studied gene families, see e.g. [19,35,54,53]. While their role in animal development is well established, their role in evolution is less well understood, see e.g.…”

Section: Introductionmentioning

confidence: 99%

The duplication of the Hox gene clusters in teleost fishes*1

Prohaska

Stadler

2004

Theory in Biosciences

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Higher teleost fishes, including zebrafish and fugu, have duplicated their Hox genes relative to the gene inventory of other gnathostome lineages. The most widely accepted theory contends that the duplicate Hox clusters orginated synchronously during a single genome duplication event in the early history of ray-finned fishes. In this contribution we collect and re-evaluate all publicly available sequence information. In particular, we show that the short Hox gene fragments from published PCR surveys of the killifish Fundulus heteroclitus, the medaka Oryzias latipes and the goldfish Carassius auratus can used to determine with little ambiguity not only their paralog group but also their membership in a particular cluster. Together with a survey of the genomic sequence data from the pufferfish Tetraodon nigroviridis we show that at least percomorpha, and possibly all eutelosts, share a system of seven orthologous Hox gene clusters, while at least the HoxC and HoxD clusters in ostariophysian (zebrafish) lineage might have arisen independently. There is little doubt about the orthology of the two teleost duplicates of the HoxA and HoxB clusters. A careful analysis of both the coding sequence of Hox genes and of conserved noncoding sequences provides additional support for the "duplication early" hypothesis that the Hox clusters in teleosts are derived by subsequent gene loss from an eight-cluster situation, although the data remain ambiguous in particular for the HoxC clusters. Assuming the "duplication early" hypothesis we use the new evidence on the Hox gene complements to determine the phylogenetic positions of gene-loss events in the wake of the cluster duplication. Surprisingly, we find that the resolution of redundancy seems to be a slow process that ist still-ongoing. A few suggestion on which additional sequence data would be most informative for resolving the history of the teleostean Hox genes are discussed.

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“…Because of the diversity of HTH proteins, evolutionary studies have more frequently concentrated on diversity within the approximately 23 major evolutionary lineages, or clades (e.g., Rosinski and Atchley 1998;Nguyen and Saier 1995;Sun et al 1997;Ruddle et al 1994), as opposed to studies across all known clades. The reasons for concentrating within clades are obvious.…”

Section: Introductionmentioning

confidence: 99%

Molecular Evolution of Helix–Turn–Helix Proteins

Rosinski

Atchley

1999

J Mol Evol

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Abstract. The helix-turn-helix domain-containing family of transcriptional regulators is of ancient origin and has been incorporated into numerous disparate biological processes. As a consequence, the forces shaping its early evolution have been difficult to reconstruct. Herein, we analyze this large and diverse family with a combination of traditional phylogenetic techniques and newer sequence analysis tools to determine whether the helix-turn-helix family arose from a single common ancestor. Our analyses of the DNA-binding domain show that amino acid chemistry is conserved at many sites in the first helix and the turn. The high level of divergence combined with the short length of the domain hinders robust reconstruction of the entire phylogeny, but some level of deep node inference is possible. All analyses point to a predominantly monophyletic origin for the helix-turn-helix domain. The consequences of such an origin for a diverse group of proteins, and guidelines for the identification of future members of the HTH family are discussed.

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EVOLUTION OF HOX GENES

Cited by 219 publications

References 35 publications

HOXD3-overexpression increases integrin αvβ3 expression and deprives E-cadherin while it enhances cell motility in A549 cells

HOXD3-overexpression increases integrin αvβ3 expression and deprives E-cadherin while it enhances cell motility in A549 cells

The duplication of the Hox gene clusters in teleost fishes*1

Molecular Evolution of Helix–Turn–Helix Proteins

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