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59. Ellis van Creveld2 is required for postnatal craniofacial bone development

Author

Badri, Mohammed K., Zhang, Honghao, Ohyama, Yoshio, Venkitapathi, Sundharamani, Kamiya, Nobuhiro, Takeda, Haruko, Ray, Manas, Scott, Greg, Tsuji, Takehito, Kunieda, Tetsuo, Mishina, Yuji, and Mochida, Yoshiyuki

Subjects
Mice, Knockout, Heterozygote, Bone Development, Ellis-Van Creveld Syndrome, Homozygote, Membrane Proteins, Article, Bone and Bones, Facial Bones, Craniofacial Abnormalities, Mice, Inbred C57BL, Mice, Phenotype, Animals, Newborn, Animals, Intercellular Signaling Peptides and Proteins, Female
Abstract

Ellis-van Creveld (EvC) syndrome is a genetic disorder with mutations in either EVC or EVC2 gene. Previous case studies reported that EvC patients underwent orthodontic treatment, suggesting the presence of craniofacial bone phenotypes. To investigate whether a mutation in EVC2 gene causes a craniofacial bone phenotype, Evc2 knockout (KO) mice were generated and cephalometric analysis was performed. The heads of wild type (WT), heterozygous (Het) and homozygous Evc2 KO mice (1-, 3-, and 6-week-old) were prepared and cephalometric analysis based on the selected reference points on lateral X-ray radiographs was performed. The linear and angular bone measurements were then calculated, compared between WT, Het and KO and statistically analyzed at each time point. Our data showed that length of craniofacial bones in KO was significantly lowered by ∼20% to that of WT and Het, the growth of certain bones, including nasal bone, palatal length, and premaxilla was more affected in KO, and the reduction in these bone length was more significantly enhanced at later postnatal time points (3 and 6 weeks) than early time point (1 week). Furthermore, bone-to-bone relationship to cranial base and cranial vault in KO was remarkably changed, i.e. cranial vault and nasal bone were depressed and premaxilla and mandible were developed in a more ventral direction. Our study was the first to show the cause-effect relationship between Evc2 deficiency and craniofacial defects in EvC syndrome, demonstrating that Evc2 is required for craniofacial bone development and its deficiency leads to specific facial bone growth defect. Anat Rec, 299:1110-1120, 2016. © 2016 Wiley Periodicals, Inc.

Published
2016

61. Generation of Evc2/Limbin global and conditional KO mice and its roles during mineralized tissue formation

Author

Zhang, Honghao, Takeda, Haruko, Tsuji, Takehito, Kamiya, Nobuhiro, Rajderkar, Sudha, Louie, Ke’ Ale, Collier, Crystal, Scott, Greg, Ray, Manas, Mochida, Yoshiyuki, Kaartinen, Vesa, Kunieda, Tetsuo, and Mishina, Yuji

Subjects
Article
Abstract

Ellis-van Creveld (EvC) syndrome (OMIM 225500) is an autosomal recessive disease characterized with chondrodysplastic dwarfism in association with abnormalities in oral cavity. Ciliary proteins EVC and EVC2 have been identified as causative genes and they play an important role on Hedgehog signal transduction. We have also identified a causative gene LIMBIN for bovine chondrodysplastic dwarfism (bcd) that is later identified as the bovine ortholog of EVC2. Here, we report generation of conventional and conditional mutant Evc2/Limbin alleles that mimics mutations found in EvC patients and bcd cattle. Resulted homozygous mice showed no ciliary localization of EVC2 and EVC and displayed reduced Hedgehog signaling activity in association with skeletal and oral defects similar to the EvC patients. Cartilage-specific disruption of Evc2/Limbin resulted in similar but milder skeletal defects, whereas osteoblast-specific disruption did not cause overt changes in skeletal system. Neural crest-specific disruption of Evc2/Limbin resulted in defective incisor growth similar to that seen in conventional knockouts; however, differentiation of amelobolasts was relatively normal in the conditional knockouts. These results showcased functions of EVC2/LIMBIN during formation of mineralized tissues. Availability of the conditional allele for this gene should facilitate further detailed analyses of the role of EVC2/LIMBIN in pathogenesis of EvC syndrome. genesis 53:612-626, 2015. © 2015 Wiley Periodicals, Inc.

Published
2015

66. Ellis Van Creveld2 is Required for Postnatal Craniofacial Bone Development

Author

Badri, Mohammed K., primary, Zhang, Honghao, additional, Ohyama, Yoshio, additional, Venkitapathi, Sundharamani, additional, Kamiya, Nobuhiro, additional, Takeda, Haruko, additional, Ray, Manas, additional, Scott, Greg, additional, Tsuji, Takehito, additional, Kunieda, Tetsuo, additional, Mishina, Yuji, additional, and Mochida, Yoshiyuki, additional

Published
2016
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67. Hybrid Sterility with Meiotic Metaphase Arrest in Intersubspecific Mouse Crosses.

Author

Nishino, Risako, Petri, Sabrina, Handel, Mary Ann, Kunieda, Tetsuo, and Fujiwara, Yasuhiro

Subjects
ORGANISMS, SPECIES, GAMETOGENESIS, INFERTILITY, MAMMALS, CHROMOSOMES, GAMETES
Abstract

Although organisms belonging to different species and subspecies sometimes produce fertile offspring, a hallmark of the speciation process is reproductive isolation, characterized by hybrid sterility (HS) due to failure in gametogenesis. In mammals, HS is usually exhibited by males, the heterogametic sex. The phenotypic manifestations of HS are complex. The most frequently observed are abnormalities in both autosomal and sex chromosome interactions that are linked to meiotic prophase arrest or postmeiotic spermiogenesis aberrations and lead to defective or absent gametes. The aim of this study was to determine the HS phenotypes in intersubspecific F1 mice produced by matings between Mus musculus molossinus -derived strains and diverse Mus musculus domesticus -inbred laboratory mouse strains. Most of these crosses produced fertile F1 offspring. However, when female BALB/cJ (domesticus) mice were mated to male JF1/MsJ (molossinus) mice, the (BALB dom xJF1 mol )F1 males were sterile, whereas the (JF1 mol xBALB dom )F1 males produced by the reciprocal crossings were fertile; thus the sterility phenotype was asymmetric. The sterile (BALB dom xJF1 mol ) F1 males exhibited a high rate of meiotic metaphase arrest with misaligned chromosomes, probably related to a high frequency of XY dissociation. Intriguingly, in the sterile (BALB dom xJF1 mol )F1 males we observed aberrant allele-specific expression of several meiotic genes, that play critical roles in important meiotic events including chromosome pairing. Together, these observations of an asymmetrical HS phenotype in intersubspecific F1 males, probably owing to meiotic defects in the meiotic behavior of the XY chromosomes pair and possibly also transcriptional misregulation of meiotic genes, provide new models and directions for understanding speciation mechanisms in mammals. [ABSTRACT FROM AUTHOR]

Published
2019
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68. Liver transplantation: New treatment for mucopolysaccharidosis type VI in rats.

Author

Toyama, Sumika, Migita, Ohsuke, Fujino, Masayuki, Kunieda, Tetsuo, Kosuga, Motomichi, Fukuhara, Yasuyuki, Nagahara, Yukitoshi, Li, Xiao‐Kang, and Okuyama, Torayuki

Subjects
SKULL radiography, HEART analysis, ANIMAL experimentation, BLOOD testing, FACIAL bones, GLYCOSAMINOGLYCANS, HISTOLOGICAL techniques, KNEE, LIVER transplantation, MUCOPOLYSACCHARIDOSIS, RATS, SPLEEN, TREATMENT effectiveness
Abstract

Background: Mucopolysaccharidosis (MPS) VI is a rare, autosomal recessive congenital metabolic disorder caused by deficient activity of the lysosomal metabolic enzyme, N‐acetylgalactosamine 4‐sulfatase. Enzyme replacement therapy (ERT) is the current treatment for MPS VI, although it involves limited compliance to the therapy and high cost. The aim of this study was to develop a new method of treatment by conducting an orthotopic liver transplantation (LTx) using an animal model of human MPS VI, and to evaluate and examine its effectiveness for treating MPS VI. Methods: LTx was carried out from normal unaffected to affected MPS VI rats (MPR), which were then killed after LTx, and tissues from the heart, spleen, and knee joint, as well as serum, collected for biological and morphologic evaluation. Results: Liver‐transplanted (LTx) MPR had the same level of N‐acetylgalactosamine 4‐sulfatase activity in the liver and lungs as normal unaffected MPR, and the urinary secretion of mucopolysaccharides/glycosaminoglycan (GAG) in LTx MPR was significantly decreased. Furthermore, on histopathology, the spleens of LTx MPR showed elimination of vacuole cells. In the knee joints, growth plates became thinner, and on radiography the facial and cranial bones of LTx MPR were morphologically normal. Conclusions: LTx from normal to affected MPR was effective for symptoms of MPS and accumulation of GAG, suggesting that LTx could be a promising alternative approach for MPS VI. [ABSTRACT FROM AUTHOR]

Published
2019
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69. t-SNARE Syntaxin2 (STX2) Is Implicated in Intracellular Transport of Sulfoglycolipids During Meiotic Prophase in Mouse Spermatogenesis1

Author

Fujiwara, Yasuhiro, Ogonuki, Narumi, Inoue, Kimiko, Ogura, Atsuo, Handel, Mary Ann, Noguchi, Junko, and Kunieda, Tetsuo

Subjects
Male, Mice, Knockout, Mice, Spermatocytes, Animals, Golgi Apparatus, Syntaxin 1, Biological Transport, Articles, Glycolipids, Meiotic Prophase I, Spermatogenesis
Abstract

Syntaxin2 (STX2), also known as epimorphin, is a member of the SNARE family of proteins, with expression in various types of cells. We previously identified an ENU-induced mutation, repro34, in the mouse Stx2 gene. The Stx2(repro34) mutation causes male-restricted infertility due to syncytial multinucleation of spermatogenic cells during meiotic prophase. A similar phenotype is also observed in mice with targeted inactivation of Stx2, as well as in mice lacking enzymes involved in sulfoglycolipid synthesis. Herein we analyzed expression and subcellular localization of STX2 and sulfoglycolipids in spermatogenesis. The STX2 protein localizes to the cytoplasm of germ cells at the late pachytene stage. It is found in a distinct subcellular pattern, presumably in the Golgi apparatus of pachytene/diplotene spermatocytes. Sulfoglycolipids are produced in the Golgi apparatus and transported to the plasma membrane. In Stx2(repro34) mutants, sulfoglycolipids are aberrantly localized in both pachytene/diplotene spermatocytes and in multinucleated germ cells. These results suggest that STX2 plays roles in transport and/or subcellular distribution of sulfoglycolipids. STX2 function in the Golgi apparatus and sulfoglycolipids may be essential for maintenance of the constriction between neighboring developing spermatocytes, which ensures ultimate individualization of germ cells in later stages of spermatogenesis.

Published
2013

71. CNP Receptor Gene (Npr2) is Involved in the Regulation of Blood-Testis Barrier and Spermatogenesis in Mouse

Author

Sogawa, Chizuru, Tsukamoto, Satoshi, Ishida, Yuka, Yoshii, Yukie, Furukawa, Takako, KUNIEDA, Tetsuo, Saga, Tsuneo, and et.al

Abstract

C-type natriuretic peptide (CNP) exerts its main biological effects by binding to natriuretic peptide receptor B (NPR-B), a membrane-bound guanylyl cyclase receptor that produces cyclic guanosine monophosphate (cGMP). It was previously reported that cGMP induced by nitric oxide via soluble guanylyl cyclase regulates Sertoli cell tight junction in vitro and permeability of the blood-testis barrier (BTB) which separates the seminiferous epithelium into the adluminal and basal compartments during spermatogenesis. Furthermore, it was also reported that CNP regulates BTB dynamics in adult rat testes. We recently reported that the short-limbed dwarfism (SLW) mouse has a mutation in Npr-2 gene, which encodes NPR-B and this mutation results in deletion of the intracellular domain of NPR-B. However, the effect of the flaw in the NPR-B-induced cGMP production through CNP signal against spermatogenesis has not yet been demonstrated. Therefore, the aim of this study is to elucidate the function of NPR-B in the progression of spermatogenesis in mouse. We first examined the immunohistochemical distribution of NPR-B in the seminiferous epithelium of the normal mouse testis during the first-wave of spermatogenesis. NPR-B was initially expressed within a spermatogonium, and subsequently located to the cytoplasm of a spermatocyte and a round spermatid predominantly in the normal testes. We next examined the phenotype of testes in SLW mice. It was revealed that the testis of slw/slw homozygotes showed retardation of spermatogenic development in 2w and vacuolation in the seminiferous epithelium in 3w. Immunohistochemical staining of ZO-1, a tight junction protein revealed that BTB was located in a boundary between the basement and the lumen in the seminiferous epithelium of 2w normal testis, whereas BTB formation was disordered and misaligned in the 2w slw/slw. These results suggest that NPR-B mediated cGMP production through CNP signal has a role important for BTB regulation which is required for spermatogenesis., 58th/60th NIBB Conferenc

Published
2012

73. Generation ofEvc2/Limbinglobal and conditional KO mice and its roles during mineralized tissue formation

Author

Zhang, Honghao, primary, Takeda, Haruko, additional, Tsuji, Takehito, additional, Kamiya, Nobuhiro, additional, Rajderkar, Sudha, additional, Louie, Ke'Ale, additional, Collier, Crystal, additional, Scott, Greg, additional, Ray, Manas, additional, Mochida, Yoshiyuki, additional, Kaartinen, Vesa, additional, Kunieda, Tetsuo, additional, and Mishina, Yuji, additional

Published
2015
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74. Genotype distribution and allele frequencies of the genes associated with body composition and locomotion traits in Myanmar native horses.

Author

Okuda, Yu, Moe, Hla Hla, Moe, Kyaw Kyaw, Shimizu, Yuki, Nishioka, Kenji, Shimogiri, Takeshi, Mannen, Hideyuki, Kanemaki, Misao, and Kunieda, Tetsuo

Subjects
GENE frequency, HORSES, ANIMAL locomotion, BODY composition
Abstract

Myanmar native horses are small horses used mainly for drafting carts or carriages in rural areas and packing loads in mountainy areas. In the present study, we investigated genotype distributions and allele frequencies of the LCORL/ NCAPG, MSTN and DMRT3 genes, which are associated with body composition and locomotion traits of horses, in seven local populations of Myanmar native horses. The genotyping result of LCORL/ NCAPG showed that allele frequencies of C allele associated with higher withers height ranged from 0.08 to 0.27, and 0.13 in average. For MSTN, allele frequencies of C allele associated with higher proportion of Type 2B muscular fiber ranged from 0.05 to 0.23, and 0.09 in average. For DMRT3, allele frequencies of A allele associated with ambling gait ranged from 0 to 0.04, and 0.01 in average. The presences of the minor alleles of these genes at low frequencies suggest a possibility that these horse populations have not been under strong selection pressure for particular locomotion traits and body composition. Our findings of the presence of these minor alleles in Southeast Asian native horses are also informative for considering the origins of these minor alleles associated with body composition and locomotion traits in horse populations. [ABSTRACT FROM AUTHOR]

Published
2017
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76. Tudor domain containing 12 (TDRD12) is essential for secondary PIWI interacting RNA biogenesis in mice.

Author

20378889, 10295694, Pandey, Radha Raman, Tokuzawa, Yoshimi, Yang, Zhaolin, Hayashi, Eri, Ichisaka, Tomoko, Kajita, Shimpei, Asano, Yuka, Kunieda, Tetsuo, Sachidanandam, Ravi, Chuma, Shinichiro, Yamanaka, Shinya, Pillai, Ramesh S, 20378889, 10295694, Pandey, Radha Raman, Tokuzawa, Yoshimi, Yang, Zhaolin, Hayashi, Eri, Ichisaka, Tomoko, Kajita, Shimpei, Asano, Yuka, Kunieda, Tetsuo, Sachidanandam, Ravi, Chuma, Shinichiro, Yamanaka, Shinya, and Pillai, Ramesh S

Abstract

Piwi-interacting RNAs (piRNAs) are gonad-specific small RNAs that provide defense against transposable genetic elements called transposons. Our knowledge of piRNA biogenesis is sketchy, partly due to an incomplete inventory of the factors involved. Here, we identify Tudor domain-containing 12 (TDRD12; also known as ECAT8) as a unique piRNA biogenesis factor in mice. TDRD12 is detected in complexes containing Piwi protein MILI (PIWIL2), its associated primary piRNAs, and TDRD1, all of which are already implicated in secondary piRNA biogenesis. Male mice carrying either a nonsense point mutation (reproductive mutant 23 or repro23 mice) or a targeted deletion in the Tdrd12 locus are infertile and derepress retrotransposons. We find that TDRD12 is dispensable for primary piRNA biogenesis but essential for production of secondary piRNAs that enter Piwi protein MIWI2 (PIWIL4). Cell-culture studies with the insect ortholog of TDRD12 suggest a role for the multidomain protein in mediating complex formation with other participants during secondary piRNA biogenesis.

Published
2013

77. Skeletal analysis of the long bone abnormality (lbab/lbab) mouse, a novel chondrodysplastic C-type natriuretic peptide mutant.

Author

50378642, 50537347, Kondo, Eri, Yasoda, Akihiro, Tsuji, Takehito, Fujii, Toshihito, Miura, Masako, Kanamoto, Naotestu, Tamura, Naohisa, Arai, Hiroshi, Kunieda, Tetsuo, Nakao, Kazuwa, 50378642, 50537347, Kondo, Eri, Yasoda, Akihiro, Tsuji, Takehito, Fujii, Toshihito, Miura, Masako, Kanamoto, Naotestu, Tamura, Naohisa, Arai, Hiroshi, Kunieda, Tetsuo, and Nakao, Kazuwa

Abstract

Long bone abnormality (lbab/lbab) is a strain of dwarf mice. Recent studies revealed that the phenotype is caused by a spontaneous mutation in the Nppc gene, which encodes mouse C-type natriuretic peptide (CNP). In this study, we analyzed the chondrodysplastic skeletal phenotype of lbab/lbab mice. At birth, lbab/lbab mice are only slightly shorter than their wild-type littermates. Nevertheless, lbab/lbab mice do not undergo a growth spurt, and their final body and bone lengths are only ~60% of those of wild-type mice. Histological analysis revealed that the growth plate in lbab/lbab mice, especially the hypertrophic chondrocyte layer, was significantly thinner than in wild-type mice. Overexpression of CNP in the cartilage of lbab/lbab mice restored their thinned growth plate, followed by the complete rescue of their impaired endochondral bone growth. Furthermore, the bone volume in lbab/lbab mouse was severely decreased and was recovered by CNP overexpression. On the other hand, the thickness of the growth plate of lbab/+ mice was not different from that of wild-type mice; accordingly, impaired endochondral bone growth was not observed in lbab/+ mice. In organ culture experiments, tibial explants from fetal lbab/lbab mice were significantly shorter than those from lbab/+ mice and elongated by addition of 10(-7) M CNP to the same extent as lbab/+ tibiae treated with the same dose of CNP. These results demonstrate that lbab/lbab is a novel mouse model of chondrodysplasia caused by insufficient CNP action on endochondral ossification.

Published
2012

80. Allelic distributions of genes involved in economical traits, hereditary disorder, and coat color in a population of Kuchinoshima cattle

Author

SIQIN, TUYA, primary, NISHIMAKI, Takahiro, additional, IBI, Takayuki, additional, TSUJI, Takehito, additional, YONEDA, Kazuhiro, additional, OSHIMA, Ichiro, additional, KATAHIRA, Kiyomi, additional, MANNEN, Hideyuki, additional, SHIMOGIRI, Takeshi, additional, KANEMAKI, Misao, additional, and KUNIEDA, Tetsuo, additional

Published
2014
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83. Allelic frequencies and association with carcass traits of six genes in local subpopulations of Japanese Black cattle.

Author

Nishimaki, Takahiro, Ibi, Takayuki, Siqintuya, Kobayashi, Naohiko, Matsuhashi, Tamako, Akiyama, Takayuki, Yoshida, Emi, Imai, Kazumi, Matsui, Mayu, Uemura, Keiichi, Eto, Hisayoshi, Watanabe, Naoto, Fujita, Tatsuo, Saito, Yosuke, Komatsu, Tomohiko, Hoshiba, Hiroshi, Mannen, Hideyuki, Sasazaki, Shinji, and Kunieda, Tetsuo

Subjects
CATTLE carcasses, ALLELES, GENOTYPES, PHENOTYPES, ANIMAL coloration
Abstract

Marker-assisted selection (MAS) is expected to accelerate the genetic improvement of Japanese Black cattle. However, verification of the effects of the genes for MAS in different subpopulations is required prior to the application of MAS. In this study, we investigated the allelic frequencies and genotypic effects for carcass traits of six genes, which can be used in MAS, in eight local subpopulations. These genes are SCD, FASN and SREBP1, which are associated with the fatty acid composition of meat, and NCAPG, MC1R and F11, which are associated with carcass weight, coat color and blood coagulation abnormality, respectively. The frequencies of desirable alleles of SCD and FASN were relatively high and that of NCAPG was relatively low, and NCAPG was significantly associated with several carcass traits, including carcass weight. The proportions of genotypic variance explained by NCAPG to phenotypic variance were 4.83 for carcass weight. We thus confirmed that NCAPG is a useful marker for selection of carcass traits in these subpopulations. In addition, we found that the desirable alleles of six genes showed no negative effects on carcass traits. Therefore, selection using these genes to improve target traits should not have negative impacts on carcass traits. [ABSTRACT FROM AUTHOR]

Published
2016
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84. The assessment of genetic diversity within and among the eight subpopulations of Japanese Black cattle using 52 microsatellite markers

Author

Nishimaki, Takahiro, primary, Ibi, Takayuki, additional, Tanabe, Yoshihiro, additional, Miyazaki, Yoshiyuki, additional, Kobayashi, Naohiko, additional, Matsuhashi, Tamako, additional, Akiyama, Takayuki, additional, Yoshida, Emi, additional, Imai, Kazumi, additional, Matsui, Mayu, additional, Uemura, Keiichi, additional, Watanabe, Naoto, additional, Fujita, Tatsuo, additional, Saito, Yosuke, additional, Komatsu, Tomohiko, additional, Yamada, Takahisa, additional, Mannen, Hideyuki, additional, Sasazaki, Shinji, additional, and Kunieda, Tetsuo, additional

Published
2013
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92. Expression Analysis of MIF4GD in the Rat Testis

Author

OKADA, Kenzo, primary, KIMURA, Masanori, additional, MORIYAMA, Yusuke, additional, NAKAI, Michiko, additional, KIKUCHI, Kazuhiro, additional, KANEKO, Hiroyuki, additional, KUNIEDA, Tetsuo, additional, BABA, Tadashi, additional, and NOGUCHI, Junko, additional

Published
2011
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99. A New ENU-Induced Mutant Mouse with Defective Spermatogenesis Caused by a Nonsense Mutation of the Syntaxin 2/Epimorphin (Stx2/Epim) Gene

Author

AKIYAMA, Kouyou, primary, AKIMARU, Shiho, additional, ASANO, Yuka, additional, KHALAJ, Maryam, additional, KIYOSU, Chiyo, additional, MASOUDI, Ali Akbar, additional, TAKAHASHI, Sakino, additional, KATAYAMA, Kentaro, additional, TSUJI, Takehito, additional, NOGUCHI, Junko, additional, and KUNIEDA, Tetsuo, additional

Published
2008
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