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Hox transcription factors: modulators of cell-cell and cell-extracellular matrix adhesion.

Taniguchi Y - Biomed Res Int (2014)

Bottom Line: Hox genes encode homeodomain-containing transcription factors that determine cell and tissue identities in the embryo during development.Hox genes are also expressed in various adult tissues and cancer cells.In this review, the potential roles Hox proteins play in cell adhesion and migration during vertebrate body patterning are discussed.

View Article: PubMed Central - PubMed

Affiliation: Division of Basic Molecular Science and Molecular Medicine, School of Medicine, Tokai University, Isehara, Kanagawa 259-1193, Japan.

ABSTRACT
Hox genes encode homeodomain-containing transcription factors that determine cell and tissue identities in the embryo during development. Hox genes are also expressed in various adult tissues and cancer cells. In Drosophila, expression of cell adhesion molecules, cadherins and integrins, is regulated by Hox proteins operating in hierarchical molecular pathways and plays a crucial role in segment-specific organogenesis. A number of studies using mammalian cultured cells have revealed that cell adhesion molecules responsible for cell-cell and cell-extracellular matrix interactions are downstream targets of Hox proteins. However, whether Hox transcription factors regulate expression of cell adhesion molecules during vertebrate development is still not fully understood. In this review, the potential roles Hox proteins play in cell adhesion and migration during vertebrate body patterning are discussed.

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Related in: MedlinePlus

Reduced N-cadherin expression induced by HOXD3 overexpression in the roof plate of the early mouse embryo. (a, b) Expression of lacZ and HOXD3 genes in transverse neural tube sections at the thoracic level of 12.5-day transgenic embryos. Transgenic embryos were generated, in which lacZ and HOXD3 are expressed in the roof plate cells under the control of the Wnt1 regulatory element [34]. These embryos were sectioned and analyzed using in situ hybridization. Expression of lacZ (control) is restricted to roof plate cells within the neural tube, while HOXD3 expression is localized not only in the dorsal neural tube, but also within the ventricular zone and in ventral regions of the neural tube. (c, d) N-Cadherin expression in the thoracic neural tubes of 12.5-day lacZ- and HOXD3-expressing transgenic embryos. Transverse sections were stained using anti-human N-cadherin antibodies [34]. N-Cadherin is strongly expressed in the ventricular zone of lacZ-expressing embryos, whereas the ventricular zone in HOXD3-expressing embryos is composed of a number of progenitor cells that do not express N-cadherin. The ventricular zone is surrounded by dotted lines. Insets show that N-cadherin expression levels in the sympathetic ganglia of lacZ-expressing embryos are similar to those of HOXD3-expressing embryos. (e, f) Summary of the neural tube phenotype in transgenic embryos expressing lacZ and HOXD3. In embryos expressing lacZ, N-cadherin expression (green) is distributed throughout the neural tube. In HOXD3-expressing embryos, roof plate cells expressing HOXD3 (red circles) expand ventrally into the ventricular zone, where almost all N-cadherin-expressing cells are lost. R, roof plate; IZ, intermediate zone; VZ, ventricular zone. Scale bar: 100 μm.
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fig3: Reduced N-cadherin expression induced by HOXD3 overexpression in the roof plate of the early mouse embryo. (a, b) Expression of lacZ and HOXD3 genes in transverse neural tube sections at the thoracic level of 12.5-day transgenic embryos. Transgenic embryos were generated, in which lacZ and HOXD3 are expressed in the roof plate cells under the control of the Wnt1 regulatory element [34]. These embryos were sectioned and analyzed using in situ hybridization. Expression of lacZ (control) is restricted to roof plate cells within the neural tube, while HOXD3 expression is localized not only in the dorsal neural tube, but also within the ventricular zone and in ventral regions of the neural tube. (c, d) N-Cadherin expression in the thoracic neural tubes of 12.5-day lacZ- and HOXD3-expressing transgenic embryos. Transverse sections were stained using anti-human N-cadherin antibodies [34]. N-Cadherin is strongly expressed in the ventricular zone of lacZ-expressing embryos, whereas the ventricular zone in HOXD3-expressing embryos is composed of a number of progenitor cells that do not express N-cadherin. The ventricular zone is surrounded by dotted lines. Insets show that N-cadherin expression levels in the sympathetic ganglia of lacZ-expressing embryos are similar to those of HOXD3-expressing embryos. (e, f) Summary of the neural tube phenotype in transgenic embryos expressing lacZ and HOXD3. In embryos expressing lacZ, N-cadherin expression (green) is distributed throughout the neural tube. In HOXD3-expressing embryos, roof plate cells expressing HOXD3 (red circles) expand ventrally into the ventricular zone, where almost all N-cadherin-expressing cells are lost. R, roof plate; IZ, intermediate zone; VZ, ventricular zone. Scale bar: 100 μm.

Mentions: When neural crest cells delaminate from the dorsal neural tube by EMT, these cells lose N-cadherin on their surfaces. [73–75]. As mentioned previously, HOXD3 promotes cell motile activity and invasiveness in lung cancer cells [33]. To investigate whether HOXD3 expression regulates cell adhesiveness in dorsal neural tube or roof plate cells in the early mouse embryo, transgenic mouse embryos were generated that overexpress HOXD3 in these cell types under the control of the Wnt1 regulatory element [34]. Dorsal neural tube cells expressing HOXD3 expand ventrally within the neural tube (Figures 3(a), 3(b), 3(e), and 3(f)). This finding raises the possibility that HOXD3-expressing roof plate cells propagate in the dorsal neural tube and then migrate ventrally. Furthermore, in the neural tube ventricular zone, a large number of progenitor cells that do not express N-cadherin protein can be observed in HOXD3-expressing transgenic embryos (Figures 3(c), 3(d), 3(e), and 3(f)). Although HOXD3 expression is localized in the dorsal half of the neural tube and in cells immediately adjacent to the floor plate, progenitor cells that do not express N-cadherin are distributed throughout the ventricular zone. This finding indicates that HOXD3 expression has a non-cell-autonomous effect, negatively affecting N-cadherin expression in cells at a distance from those expressing HOXD3. Therefore, signaling molecules or secreted proteins whose expression is induced by HOXD3 likely reduce N-cadherin expression.


Hox transcription factors: modulators of cell-cell and cell-extracellular matrix adhesion.

Taniguchi Y - Biomed Res Int (2014)

Reduced N-cadherin expression induced by HOXD3 overexpression in the roof plate of the early mouse embryo. (a, b) Expression of lacZ and HOXD3 genes in transverse neural tube sections at the thoracic level of 12.5-day transgenic embryos. Transgenic embryos were generated, in which lacZ and HOXD3 are expressed in the roof plate cells under the control of the Wnt1 regulatory element [34]. These embryos were sectioned and analyzed using in situ hybridization. Expression of lacZ (control) is restricted to roof plate cells within the neural tube, while HOXD3 expression is localized not only in the dorsal neural tube, but also within the ventricular zone and in ventral regions of the neural tube. (c, d) N-Cadherin expression in the thoracic neural tubes of 12.5-day lacZ- and HOXD3-expressing transgenic embryos. Transverse sections were stained using anti-human N-cadherin antibodies [34]. N-Cadherin is strongly expressed in the ventricular zone of lacZ-expressing embryos, whereas the ventricular zone in HOXD3-expressing embryos is composed of a number of progenitor cells that do not express N-cadherin. The ventricular zone is surrounded by dotted lines. Insets show that N-cadherin expression levels in the sympathetic ganglia of lacZ-expressing embryos are similar to those of HOXD3-expressing embryos. (e, f) Summary of the neural tube phenotype in transgenic embryos expressing lacZ and HOXD3. In embryos expressing lacZ, N-cadherin expression (green) is distributed throughout the neural tube. In HOXD3-expressing embryos, roof plate cells expressing HOXD3 (red circles) expand ventrally into the ventricular zone, where almost all N-cadherin-expressing cells are lost. R, roof plate; IZ, intermediate zone; VZ, ventricular zone. Scale bar: 100 μm.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4127299&req=5

fig3: Reduced N-cadherin expression induced by HOXD3 overexpression in the roof plate of the early mouse embryo. (a, b) Expression of lacZ and HOXD3 genes in transverse neural tube sections at the thoracic level of 12.5-day transgenic embryos. Transgenic embryos were generated, in which lacZ and HOXD3 are expressed in the roof plate cells under the control of the Wnt1 regulatory element [34]. These embryos were sectioned and analyzed using in situ hybridization. Expression of lacZ (control) is restricted to roof plate cells within the neural tube, while HOXD3 expression is localized not only in the dorsal neural tube, but also within the ventricular zone and in ventral regions of the neural tube. (c, d) N-Cadherin expression in the thoracic neural tubes of 12.5-day lacZ- and HOXD3-expressing transgenic embryos. Transverse sections were stained using anti-human N-cadherin antibodies [34]. N-Cadherin is strongly expressed in the ventricular zone of lacZ-expressing embryos, whereas the ventricular zone in HOXD3-expressing embryos is composed of a number of progenitor cells that do not express N-cadherin. The ventricular zone is surrounded by dotted lines. Insets show that N-cadherin expression levels in the sympathetic ganglia of lacZ-expressing embryos are similar to those of HOXD3-expressing embryos. (e, f) Summary of the neural tube phenotype in transgenic embryos expressing lacZ and HOXD3. In embryos expressing lacZ, N-cadherin expression (green) is distributed throughout the neural tube. In HOXD3-expressing embryos, roof plate cells expressing HOXD3 (red circles) expand ventrally into the ventricular zone, where almost all N-cadherin-expressing cells are lost. R, roof plate; IZ, intermediate zone; VZ, ventricular zone. Scale bar: 100 μm.
Mentions: When neural crest cells delaminate from the dorsal neural tube by EMT, these cells lose N-cadherin on their surfaces. [73–75]. As mentioned previously, HOXD3 promotes cell motile activity and invasiveness in lung cancer cells [33]. To investigate whether HOXD3 expression regulates cell adhesiveness in dorsal neural tube or roof plate cells in the early mouse embryo, transgenic mouse embryos were generated that overexpress HOXD3 in these cell types under the control of the Wnt1 regulatory element [34]. Dorsal neural tube cells expressing HOXD3 expand ventrally within the neural tube (Figures 3(a), 3(b), 3(e), and 3(f)). This finding raises the possibility that HOXD3-expressing roof plate cells propagate in the dorsal neural tube and then migrate ventrally. Furthermore, in the neural tube ventricular zone, a large number of progenitor cells that do not express N-cadherin protein can be observed in HOXD3-expressing transgenic embryos (Figures 3(c), 3(d), 3(e), and 3(f)). Although HOXD3 expression is localized in the dorsal half of the neural tube and in cells immediately adjacent to the floor plate, progenitor cells that do not express N-cadherin are distributed throughout the ventricular zone. This finding indicates that HOXD3 expression has a non-cell-autonomous effect, negatively affecting N-cadherin expression in cells at a distance from those expressing HOXD3. Therefore, signaling molecules or secreted proteins whose expression is induced by HOXD3 likely reduce N-cadherin expression.

Bottom Line: Hox genes encode homeodomain-containing transcription factors that determine cell and tissue identities in the embryo during development.Hox genes are also expressed in various adult tissues and cancer cells.In this review, the potential roles Hox proteins play in cell adhesion and migration during vertebrate body patterning are discussed.

View Article: PubMed Central - PubMed

Affiliation: Division of Basic Molecular Science and Molecular Medicine, School of Medicine, Tokai University, Isehara, Kanagawa 259-1193, Japan.

ABSTRACT
Hox genes encode homeodomain-containing transcription factors that determine cell and tissue identities in the embryo during development. Hox genes are also expressed in various adult tissues and cancer cells. In Drosophila, expression of cell adhesion molecules, cadherins and integrins, is regulated by Hox proteins operating in hierarchical molecular pathways and plays a crucial role in segment-specific organogenesis. A number of studies using mammalian cultured cells have revealed that cell adhesion molecules responsible for cell-cell and cell-extracellular matrix interactions are downstream targets of Hox proteins. However, whether Hox transcription factors regulate expression of cell adhesion molecules during vertebrate development is still not fully understood. In this review, the potential roles Hox proteins play in cell adhesion and migration during vertebrate body patterning are discussed.

Show MeSH
Related in: MedlinePlus