The Experts below are selected from a list of 16467 Experts worldwide ranked by ideXlab platform
Yuuta Moriyama - One of the best experts on this subject based on the ideXlab platform.
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Evolution and development of the homocercal Caudal Fin in teleosts.
Development growth & differentiation, 2013Co-Authors: Yuuta Moriyama, Hiroyuki TakedaAbstract:The vertebrate Caudal skeleton is one of the most innovative structures in vertebrate evolution and has been regarded as an excellent model for functional morphology, a discipline that relates a structure to its function. Teleosts have an internally-asymmetrical Caudal Fin, called the homocercal Caudal Fin, formed by the upward bending of the Caudal-most portion of the body axis, the ural region. This homocercal type of the Caudal Fin ensures powerful and complex locomotion and is thought to be one of the most important evolutionary innovations for teleosts during adaptive radiation in an aquatic environment. In this review, we summarize the past and present research of fish Caudal skeletons, especially focusing on the homocercal Caudal Fin seen in teleosts. A series of studies with a medaka spontaneous mutant have provided important insight into the evolution and development of the homocercal Caudal skeleton. By comparing developmental processes in various vertebrates, we propose a scenario for acquisition and morphogenesis of the homocercal Caudal skeleton during vertebrate evolution.
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the medaka zic1 zic4 mutant provides molecular insights into teleost Caudal Fin evolution
Current Biology, 2012Co-Authors: Yuuta Moriyama, Toru Kawanishi, Ryohei Nakamura, Tatsuya Tsukahara, Kenta Sumiyama, Maximiliano L. Suster, Koichi Kawakami, Atsushi Toyoda, Asao FujiyamaAbstract:Summary Teleosts have an asymmetrical Caudal Fin skeleton formed by the upward bending of the Caudal-most portion of the body axis, the ural region [1–3]. This homocercal type of Caudal Fin ensures powerful and complex locomotion and is regarded as one of the most important innovations for teleosts during adaptive radiation in an aquatic environment [4–6]. However, the mechanisms that create asymmetric Caudal Fin remain largely unknown. The spontaneous medaka (teleost fish) mutant, Double anal Fin ( Da ), exhibits a unique symmetrical Caudal skeleton that resembles the diphycercal type seen in Polypterus and Coelacanth. We performed a detailed analysis of the Da mutant to obtain molecular insight into Caudal Fin morphogenesis. We first demonstrate that a large transposon, inserted into the enhancer region of the zic1 and zic4 genes ( zic1/zic4 ) in Da , is associated with the mesoderm-specific loss of their transcription. We then show that zic1/zic4 are strongly expressed in the dorsal part of the ural mesenchyme and thereby induce asymmetric Caudal Fin development in wild-type embryos, whereas their expression is lost in Da . Comparative analysis further indicates that the dorsal mesoderm expression of zic1/zic4 is conserved in teleosts, highlighting the crucial role of zic1/zic4 in Caudal Fin morphogenesis.
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The Medaka zic1/zic4 Mutant Provides Molecular Insights into Teleost Caudal Fin Evolution
Current biology : CB, 2012Co-Authors: Yuuta Moriyama, Toru Kawanishi, Ryohei Nakamura, Tatsuya Tsukahara, Kenta Sumiyama, Maximiliano L. Suster, Koichi Kawakami, Atsushi Toyoda, Asao Fujiyama, Yuuri YasuokaAbstract:Summary Teleosts have an asymmetrical Caudal Fin skeleton formed by the upward bending of the Caudal-most portion of the body axis, the ural region [1–3]. This homocercal type of Caudal Fin ensures powerful and complex locomotion and is regarded as one of the most important innovations for teleosts during adaptive radiation in an aquatic environment [4–6]. However, the mechanisms that create asymmetric Caudal Fin remain largely unknown. The spontaneous medaka (teleost fish) mutant, Double anal Fin ( Da ), exhibits a unique symmetrical Caudal skeleton that resembles the diphycercal type seen in Polypterus and Coelacanth. We performed a detailed analysis of the Da mutant to obtain molecular insight into Caudal Fin morphogenesis. We first demonstrate that a large transposon, inserted into the enhancer region of the zic1 and zic4 genes ( zic1/zic4 ) in Da , is associated with the mesoderm-specific loss of their transcription. We then show that zic1/zic4 are strongly expressed in the dorsal part of the ural mesenchyme and thereby induce asymmetric Caudal Fin development in wild-type embryos, whereas their expression is lost in Da . Comparative analysis further indicates that the dorsal mesoderm expression of zic1/zic4 is conserved in teleosts, highlighting the crucial role of zic1/zic4 in Caudal Fin morphogenesis.
Jeroen Den Hertog - One of the best experts on this subject based on the ideXlab platform.
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shp2 mitogen activated protein kinase signaling drives proliferation during zebrafish embryo Caudal Fin fold regeneration
Molecular and Cellular Biology, 2017Co-Authors: Alexander James Hale, Jeroen Den HertogAbstract:Regeneration of the zebrafish Caudal Fin following amputation occurs through wound healing, followed by formation of a blastema, which produces cells to replace the lost tissue in the Final phase of regenerative outgrowth. We show that ptpn11a-/- ptpn11b-/- zebrafish embryos, lacking functional Shp2, fail to regenerate their Caudal Fin folds. Rescue experiments indicated that Shp2a has a functional signaling role, requiring its catalytic activity and SH2 domains but not the two C-terminal tyrosine phosphorylation sites. Surprisingly, expression of Shp2a variants with increased and reduced catalytic activity, respectively, rescued Caudal Fin fold regeneration to similar extents. Expression of mmp9 and junbb, indicative of formation of the wound epidermis and distal blastema, respectively, suggested that these processes occurred in ptpn11a-/- ptpn11b-/- zebrafish embryos. However, cell proliferation and MAPK phosphorylation were reduced. Pharmacological inhibition of MEK1 in wild-type zebrafish embryos phenocopied loss of Shp2. Our results suggest an essential role for Shp2a-mitogen-activated protein kinase (MAPK) signaling in promoting cell proliferation during zebrafish embryo Caudal Fin fold regeneration.
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Impaired Caudal Fin‐fold regeneration in zebrafish deficient for the tumor suppressor Pten
Regeneration (Oxford England), 2017Co-Authors: Alexander James Hale, Ali Kiai, Jelte Sikkens, Jeroen Den HertogAbstract:Zebrafish are able to completely regrow their Caudal Fin-folds after amputation. Following injury, wound healing occurs, followed by the formation of a blastema, which produces cells to replace the lost tissue in the Final phase of regenerative outgrowth. Here we show that, surprisingly, the phosphatase and tumor suppressor Pten, an antagonist of phosphoinositide-3-kinase (PI3K) signaling, is required for zebrafish Caudal Fin-fold regeneration. We found that homozygous knock-out mutant (ptena-/-ptenb-/- ) zebrafish embryos, lacking functional Pten, did not regenerate their Caudal Fin-folds. AKT phosphorylation was enhanced, which is consistent with the function of Pten. Reexpression of Pten, but not catalytically inactive mutant Pten-C124S, rescued regeneration, as did pharmacological inhibition of PI3K. Blastema formation, determined by in situ hybridization for the blastema marker junbb, appeared normal upon Caudal Fin-fold amputation of ptena-/-ptenb-/- zebrafish embryos. Whole-mount immunohistochemistry using specific markers indicated that proliferation was arrested in embryos lacking functional Pten, and that apoptosis was enhanced. Together, these results suggest a critical role for Pten by limiting PI3K signaling during the regenerative outgrowth phase of zebrafish Caudal Fin-fold regeneration.
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Differential oxidation of protein-tyrosine phosphatases during zebrafish Caudal Fin regeneration.
Scientific reports, 2017Co-Authors: Alexander James Hale, Simone Lemeer, Jeroen Den HertogAbstract:Zebrafish have the capacity to regenerate lost tissues and organs. Amputation of the Caudal Fin results in a rapid, transient increase in H2O2 levels emanating from the wound margin, which is essential for regeneration, because quenching of reactive oxygen species blocks regeneration. Protein-tyrosine phosphatases (PTPs) have a central role in cell signalling and are susceptible to oxidation, which results in transient inactivation of their catalytic activity. We hypothesized that PTPs may become oxidized in response to amputation of the Caudal Fin. Using the oxidized PTP-specific (ox-PTP) antibody and liquid chromatography-mass spectrometry, we identified 33 PTPs in adult zebrafish Fin clips of the total of 44 PTPs that can theoretically be detected based on sequence conservation. Of these 33 PTPs, 8 were significantly more oxidized 40 min after Caudal Fin amputation. Surprisingly, Shp2, one of the PTPs that were oxidized in response to Caudal Fin amputation, was required for Caudal Fin regeneration. In contrast, Rptpα, which was not oxidized upon amputation, was dispensable for Caudal Fin regeneration. Our results demonstrate that PTPs are differentially oxidized in response to Caudal Fin amputation and that there is a differential requirement for PTPs in regeneration.
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impaired Caudal Fin fold regeneration in zebrafish deficient for the tumor suppressor pten
Regeneration (Oxford England), 2017Co-Authors: Alexander James Hale, Jeroen Den Hertog, Ali Kiai, Jelte SikkensAbstract:Zebrafish are able to completely regrow their Caudal Fin-folds after amputation. Following injury, wound healing occurs, followed by the formation of a blastema, which produces cells to replace the lost tissue in the Final phase of regenerative outgrowth. Here we show that, surprisingly, the phosphatase and tumor suppressor Pten, an antagonist of phosphoinositide-3-kinase (PI3K) signaling, is required for zebrafish Caudal Fin-fold regeneration. We found that homozygous knock-out mutant (ptena-/-ptenb-/- ) zebrafish embryos, lacking functional Pten, did not regenerate their Caudal Fin-folds. AKT phosphorylation was enhanced, which is consistent with the function of Pten. Reexpression of Pten, but not catalytically inactive mutant Pten-C124S, rescued regeneration, as did pharmacological inhibition of PI3K. Blastema formation, determined by in situ hybridization for the blastema marker junbb, appeared normal upon Caudal Fin-fold amputation of ptena-/-ptenb-/- zebrafish embryos. Whole-mount immunohistochemistry using specific markers indicated that proliferation was arrested in embryos lacking functional Pten, and that apoptosis was enhanced. Together, these results suggest a critical role for Pten by limiting PI3K signaling during the regenerative outgrowth phase of zebrafish Caudal Fin-fold regeneration.
Asao Fujiyama - One of the best experts on this subject based on the ideXlab platform.
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the medaka zic1 zic4 mutant provides molecular insights into teleost Caudal Fin evolution
Current Biology, 2012Co-Authors: Yuuta Moriyama, Toru Kawanishi, Ryohei Nakamura, Tatsuya Tsukahara, Kenta Sumiyama, Maximiliano L. Suster, Koichi Kawakami, Atsushi Toyoda, Asao FujiyamaAbstract:Summary Teleosts have an asymmetrical Caudal Fin skeleton formed by the upward bending of the Caudal-most portion of the body axis, the ural region [1–3]. This homocercal type of Caudal Fin ensures powerful and complex locomotion and is regarded as one of the most important innovations for teleosts during adaptive radiation in an aquatic environment [4–6]. However, the mechanisms that create asymmetric Caudal Fin remain largely unknown. The spontaneous medaka (teleost fish) mutant, Double anal Fin ( Da ), exhibits a unique symmetrical Caudal skeleton that resembles the diphycercal type seen in Polypterus and Coelacanth. We performed a detailed analysis of the Da mutant to obtain molecular insight into Caudal Fin morphogenesis. We first demonstrate that a large transposon, inserted into the enhancer region of the zic1 and zic4 genes ( zic1/zic4 ) in Da , is associated with the mesoderm-specific loss of their transcription. We then show that zic1/zic4 are strongly expressed in the dorsal part of the ural mesenchyme and thereby induce asymmetric Caudal Fin development in wild-type embryos, whereas their expression is lost in Da . Comparative analysis further indicates that the dorsal mesoderm expression of zic1/zic4 is conserved in teleosts, highlighting the crucial role of zic1/zic4 in Caudal Fin morphogenesis.
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The Medaka zic1/zic4 Mutant Provides Molecular Insights into Teleost Caudal Fin Evolution
Current biology : CB, 2012Co-Authors: Yuuta Moriyama, Toru Kawanishi, Ryohei Nakamura, Tatsuya Tsukahara, Kenta Sumiyama, Maximiliano L. Suster, Koichi Kawakami, Atsushi Toyoda, Asao Fujiyama, Yuuri YasuokaAbstract:Summary Teleosts have an asymmetrical Caudal Fin skeleton formed by the upward bending of the Caudal-most portion of the body axis, the ural region [1–3]. This homocercal type of Caudal Fin ensures powerful and complex locomotion and is regarded as one of the most important innovations for teleosts during adaptive radiation in an aquatic environment [4–6]. However, the mechanisms that create asymmetric Caudal Fin remain largely unknown. The spontaneous medaka (teleost fish) mutant, Double anal Fin ( Da ), exhibits a unique symmetrical Caudal skeleton that resembles the diphycercal type seen in Polypterus and Coelacanth. We performed a detailed analysis of the Da mutant to obtain molecular insight into Caudal Fin morphogenesis. We first demonstrate that a large transposon, inserted into the enhancer region of the zic1 and zic4 genes ( zic1/zic4 ) in Da , is associated with the mesoderm-specific loss of their transcription. We then show that zic1/zic4 are strongly expressed in the dorsal part of the ural mesenchyme and thereby induce asymmetric Caudal Fin development in wild-type embryos, whereas their expression is lost in Da . Comparative analysis further indicates that the dorsal mesoderm expression of zic1/zic4 is conserved in teleosts, highlighting the crucial role of zic1/zic4 in Caudal Fin morphogenesis.
Koichi Kawakami - One of the best experts on this subject based on the ideXlab platform.
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the medaka zic1 zic4 mutant provides molecular insights into teleost Caudal Fin evolution
Current Biology, 2012Co-Authors: Yuuta Moriyama, Toru Kawanishi, Ryohei Nakamura, Tatsuya Tsukahara, Kenta Sumiyama, Maximiliano L. Suster, Koichi Kawakami, Atsushi Toyoda, Asao FujiyamaAbstract:Summary Teleosts have an asymmetrical Caudal Fin skeleton formed by the upward bending of the Caudal-most portion of the body axis, the ural region [1–3]. This homocercal type of Caudal Fin ensures powerful and complex locomotion and is regarded as one of the most important innovations for teleosts during adaptive radiation in an aquatic environment [4–6]. However, the mechanisms that create asymmetric Caudal Fin remain largely unknown. The spontaneous medaka (teleost fish) mutant, Double anal Fin ( Da ), exhibits a unique symmetrical Caudal skeleton that resembles the diphycercal type seen in Polypterus and Coelacanth. We performed a detailed analysis of the Da mutant to obtain molecular insight into Caudal Fin morphogenesis. We first demonstrate that a large transposon, inserted into the enhancer region of the zic1 and zic4 genes ( zic1/zic4 ) in Da , is associated with the mesoderm-specific loss of their transcription. We then show that zic1/zic4 are strongly expressed in the dorsal part of the ural mesenchyme and thereby induce asymmetric Caudal Fin development in wild-type embryos, whereas their expression is lost in Da . Comparative analysis further indicates that the dorsal mesoderm expression of zic1/zic4 is conserved in teleosts, highlighting the crucial role of zic1/zic4 in Caudal Fin morphogenesis.
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The Medaka zic1/zic4 Mutant Provides Molecular Insights into Teleost Caudal Fin Evolution
Current biology : CB, 2012Co-Authors: Yuuta Moriyama, Toru Kawanishi, Ryohei Nakamura, Tatsuya Tsukahara, Kenta Sumiyama, Maximiliano L. Suster, Koichi Kawakami, Atsushi Toyoda, Asao Fujiyama, Yuuri YasuokaAbstract:Summary Teleosts have an asymmetrical Caudal Fin skeleton formed by the upward bending of the Caudal-most portion of the body axis, the ural region [1–3]. This homocercal type of Caudal Fin ensures powerful and complex locomotion and is regarded as one of the most important innovations for teleosts during adaptive radiation in an aquatic environment [4–6]. However, the mechanisms that create asymmetric Caudal Fin remain largely unknown. The spontaneous medaka (teleost fish) mutant, Double anal Fin ( Da ), exhibits a unique symmetrical Caudal skeleton that resembles the diphycercal type seen in Polypterus and Coelacanth. We performed a detailed analysis of the Da mutant to obtain molecular insight into Caudal Fin morphogenesis. We first demonstrate that a large transposon, inserted into the enhancer region of the zic1 and zic4 genes ( zic1/zic4 ) in Da , is associated with the mesoderm-specific loss of their transcription. We then show that zic1/zic4 are strongly expressed in the dorsal part of the ural mesenchyme and thereby induce asymmetric Caudal Fin development in wild-type embryos, whereas their expression is lost in Da . Comparative analysis further indicates that the dorsal mesoderm expression of zic1/zic4 is conserved in teleosts, highlighting the crucial role of zic1/zic4 in Caudal Fin morphogenesis.
Alexander James Hale - One of the best experts on this subject based on the ideXlab platform.
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shp2 mitogen activated protein kinase signaling drives proliferation during zebrafish embryo Caudal Fin fold regeneration
Molecular and Cellular Biology, 2017Co-Authors: Alexander James Hale, Jeroen Den HertogAbstract:Regeneration of the zebrafish Caudal Fin following amputation occurs through wound healing, followed by formation of a blastema, which produces cells to replace the lost tissue in the Final phase of regenerative outgrowth. We show that ptpn11a-/- ptpn11b-/- zebrafish embryos, lacking functional Shp2, fail to regenerate their Caudal Fin folds. Rescue experiments indicated that Shp2a has a functional signaling role, requiring its catalytic activity and SH2 domains but not the two C-terminal tyrosine phosphorylation sites. Surprisingly, expression of Shp2a variants with increased and reduced catalytic activity, respectively, rescued Caudal Fin fold regeneration to similar extents. Expression of mmp9 and junbb, indicative of formation of the wound epidermis and distal blastema, respectively, suggested that these processes occurred in ptpn11a-/- ptpn11b-/- zebrafish embryos. However, cell proliferation and MAPK phosphorylation were reduced. Pharmacological inhibition of MEK1 in wild-type zebrafish embryos phenocopied loss of Shp2. Our results suggest an essential role for Shp2a-mitogen-activated protein kinase (MAPK) signaling in promoting cell proliferation during zebrafish embryo Caudal Fin fold regeneration.
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Impaired Caudal Fin‐fold regeneration in zebrafish deficient for the tumor suppressor Pten
Regeneration (Oxford England), 2017Co-Authors: Alexander James Hale, Ali Kiai, Jelte Sikkens, Jeroen Den HertogAbstract:Zebrafish are able to completely regrow their Caudal Fin-folds after amputation. Following injury, wound healing occurs, followed by the formation of a blastema, which produces cells to replace the lost tissue in the Final phase of regenerative outgrowth. Here we show that, surprisingly, the phosphatase and tumor suppressor Pten, an antagonist of phosphoinositide-3-kinase (PI3K) signaling, is required for zebrafish Caudal Fin-fold regeneration. We found that homozygous knock-out mutant (ptena-/-ptenb-/- ) zebrafish embryos, lacking functional Pten, did not regenerate their Caudal Fin-folds. AKT phosphorylation was enhanced, which is consistent with the function of Pten. Reexpression of Pten, but not catalytically inactive mutant Pten-C124S, rescued regeneration, as did pharmacological inhibition of PI3K. Blastema formation, determined by in situ hybridization for the blastema marker junbb, appeared normal upon Caudal Fin-fold amputation of ptena-/-ptenb-/- zebrafish embryos. Whole-mount immunohistochemistry using specific markers indicated that proliferation was arrested in embryos lacking functional Pten, and that apoptosis was enhanced. Together, these results suggest a critical role for Pten by limiting PI3K signaling during the regenerative outgrowth phase of zebrafish Caudal Fin-fold regeneration.
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Differential oxidation of protein-tyrosine phosphatases during zebrafish Caudal Fin regeneration.
Scientific reports, 2017Co-Authors: Alexander James Hale, Simone Lemeer, Jeroen Den HertogAbstract:Zebrafish have the capacity to regenerate lost tissues and organs. Amputation of the Caudal Fin results in a rapid, transient increase in H2O2 levels emanating from the wound margin, which is essential for regeneration, because quenching of reactive oxygen species blocks regeneration. Protein-tyrosine phosphatases (PTPs) have a central role in cell signalling and are susceptible to oxidation, which results in transient inactivation of their catalytic activity. We hypothesized that PTPs may become oxidized in response to amputation of the Caudal Fin. Using the oxidized PTP-specific (ox-PTP) antibody and liquid chromatography-mass spectrometry, we identified 33 PTPs in adult zebrafish Fin clips of the total of 44 PTPs that can theoretically be detected based on sequence conservation. Of these 33 PTPs, 8 were significantly more oxidized 40 min after Caudal Fin amputation. Surprisingly, Shp2, one of the PTPs that were oxidized in response to Caudal Fin amputation, was required for Caudal Fin regeneration. In contrast, Rptpα, which was not oxidized upon amputation, was dispensable for Caudal Fin regeneration. Our results demonstrate that PTPs are differentially oxidized in response to Caudal Fin amputation and that there is a differential requirement for PTPs in regeneration.
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impaired Caudal Fin fold regeneration in zebrafish deficient for the tumor suppressor pten
Regeneration (Oxford England), 2017Co-Authors: Alexander James Hale, Jeroen Den Hertog, Ali Kiai, Jelte SikkensAbstract:Zebrafish are able to completely regrow their Caudal Fin-folds after amputation. Following injury, wound healing occurs, followed by the formation of a blastema, which produces cells to replace the lost tissue in the Final phase of regenerative outgrowth. Here we show that, surprisingly, the phosphatase and tumor suppressor Pten, an antagonist of phosphoinositide-3-kinase (PI3K) signaling, is required for zebrafish Caudal Fin-fold regeneration. We found that homozygous knock-out mutant (ptena-/-ptenb-/- ) zebrafish embryos, lacking functional Pten, did not regenerate their Caudal Fin-folds. AKT phosphorylation was enhanced, which is consistent with the function of Pten. Reexpression of Pten, but not catalytically inactive mutant Pten-C124S, rescued regeneration, as did pharmacological inhibition of PI3K. Blastema formation, determined by in situ hybridization for the blastema marker junbb, appeared normal upon Caudal Fin-fold amputation of ptena-/-ptenb-/- zebrafish embryos. Whole-mount immunohistochemistry using specific markers indicated that proliferation was arrested in embryos lacking functional Pten, and that apoptosis was enhanced. Together, these results suggest a critical role for Pten by limiting PI3K signaling during the regenerative outgrowth phase of zebrafish Caudal Fin-fold regeneration.
