Search

Your search keyword '"Kimura-Yoshida, Chiharu"' showing total 34 results
Start Over Author "Kimura-Yoshida, Chiharu"
34 results on '"Kimura-Yoshida, Chiharu"'

11. Intrauterine Pressures Adjusted by Reichert's Membrane Are Crucial for Early Mouse Morphogenesis

Author

Ueda, Yoko, Kimura-Yoshida, Chiharu, Mochida, Kyoko, Tsume, Mami, Kameo, Yoshitaka, Adachi, Taiji, Lefebvre, Olivier, Hiramatsu, Ryuji, and Matsuo, Isao

Subjects
early mouse morphogenesis, uterine mechanical environment, atomic force microscopy, egg-cylinder morphogenesis, uterine uterine smooth muscle contractions, extracellular matrix, embryonic structures, Reichert's membrane, intrauterine pressures, micro-computed tomography, basement membrane
Abstract

Mammalian embryogenesis proceeds in utero with the support of nutrients and gases from maternal tissues. However, the contribution of the mechanical environment provided by the uterus to embryogenesis remains unaddressed. Notably, how intrauterine pressures are produced, accurately adjusted, and exerted on embryos are completely unknown. Here, we find that Reichert’s membrane, a specialized basement membrane that wraps around the implanted mouse embryo, plays a crucial role as a shock absorber to protect embryos from intrauterine pressures. Notably, intrauterine pressures are produced by uterine smooth muscle contractions, showing the highest and most frequent periodic peaks just after implantation. Mechanistically, such pressures are adjusted within the sealed space between the embryo and uterus created by Reichert’s membrane and are involved in egg-cylinder morphogenesis as an important biomechanical environment in utero. Thus, we propose the buffer space sealed by Reichert’s membrane cushions and disperses intrauterine pressures exerted on embryos for egg-cylinder morphogenesis.

Published
2020

12. Intrauterine Pressures Adjusted by Reichert's Membrane Are Crucial for Early Mouse Morphogenesis

Author

60611431, 40243323, Ueda, Yoko, Kimura-Yoshida, Chiharu, Mochida, Kyoko, Tsume, Mami, Kameo, Yoshitaka, Adachi, Taiji, Lefebvre, Olivier, Hiramatsu, Ryuji, Matsuo, Isao, 60611431, 40243323, Ueda, Yoko, Kimura-Yoshida, Chiharu, Mochida, Kyoko, Tsume, Mami, Kameo, Yoshitaka, Adachi, Taiji, Lefebvre, Olivier, Hiramatsu, Ryuji, and Matsuo, Isao

Abstract

Mammalian embryogenesis proceeds in utero with the support of nutrients and gases from maternal tissues. However, the contribution of the mechanical environment provided by the uterus to embryogenesis remains unaddressed. Notably, how intrauterine pressures are produced, accurately adjusted, and exerted on embryos are completely unknown. Here, we find that Reichert’s membrane, a specialized basement membrane that wraps around the implanted mouse embryo, plays a crucial role as a shock absorber to protect embryos from intrauterine pressures. Notably, intrauterine pressures are produced by uterine smooth muscle contractions, showing the highest and most frequent periodic peaks just after implantation. Mechanistically, such pressures are adjusted within the sealed space between the embryo and uterus created by Reichert’s membrane and are involved in egg-cylinder morphogenesis as an important biomechanical environment in utero. Thus, we propose the buffer space sealed by Reichert’s membrane cushions and disperses intrauterine pressures exerted on embryos for egg-cylinder morphogenesis.

Published
2020

13. Competition for Mitogens Regulates Spermatogenic Stem Cell Homeostasis in an Open Niche

Author

Kitadate, Yu, primary, Jörg, David J., additional, Tokue, Moe, additional, Maruyama, Ayumi, additional, Ichikawa, Rie, additional, Tsuchiya, Soken, additional, Segi-Nishida, Eri, additional, Nakagawa, Toshinori, additional, Uchida, Aya, additional, Kimura-Yoshida, Chiharu, additional, Mizuno, Seiya, additional, Sugiyama, Fumihiro, additional, Azami, Takuya, additional, Ema, Masatsugu, additional, Noda, Chiyo, additional, Kobayashi, Satoru, additional, Matsuo, Isao, additional, Kanai, Yoshiakira, additional, Nagasawa, Takashi, additional, Sugimoto, Yukihiko, additional, Takahashi, Satoru, additional, Simons, Benjamin D., additional, and Yoshida, Shosei, additional

Published
2019
Full Text
View/download PDF

14. Coordinately Co-opted Multiple Transposable Elements Constitute an Enhancer for wnt5a Expression in the Mammalian Secondary Palate

Author

Nishihara, Hidenori, Kobayashi, Naoki, Kimura-Yoshida, Chiharu, Yan, Kuo, Bormuth, Olga, Ding, Qiong, Nakanishi, Akiko, Sasaki, Takeshi, Hirakawa, Mika, Sumiyama, Kenta, Furuta, Yasuhide, Tarabykin, Victor, Matsuo, Isao, Okada, Norihiro, Nishihara, Hidenori, Kobayashi, Naoki, Kimura-Yoshida, Chiharu, Yan, Kuo, Bormuth, Olga, Ding, Qiong, Nakanishi, Akiko, Sasaki, Takeshi, Hirakawa, Mika, Sumiyama, Kenta, Furuta, Yasuhide, Tarabykin, Victor, Matsuo, Isao, and Okada, Norihiro

Abstract

Acquisition of cis-regulatory elements is a major driving force of evolution, and there are several examples of developmental enhancers derived from transposable elements (TEs). However, it remains unclear whether one enhancer element could have been produced via cooperation among multiple, yet distinct, TEs during evolution. Here we show that an evolutionarily conserved genomic region named AS3_9 comprises three TEs (AmnSINE1, X6b_DNA and MER117), inserted side-by-side, and functions as a distal enhancer for wnt5a expression during morphogenesis of the mammalian secondary palate. Functional analysis of each TE revealed step-by-step retroposition/transposition and co-option together with acquisition of a binding site for Msx1 for its full enhancer function during mammalian evolution. The present study provides a new perspective suggesting that a huge variety of TEs, in combination, could have accelerated the diversity of cis-regulatory elements involved in morphological evolution.

Published
2016

15. Coordinately Co-opted Multiple Transposable Elements Constitute an Enhancer for wnt5a Expression in the Mammalian Secondary Palate

Author

Nishihara, Hidenori, primary, Kobayashi, Naoki, additional, Kimura-Yoshida, Chiharu, additional, Yan, Kuo, additional, Bormuth, Olga, additional, Ding, Qiong, additional, Nakanishi, Akiko, additional, Sasaki, Takeshi, additional, Hirakawa, Mika, additional, Sumiyama, Kenta, additional, Furuta, Yasuhide, additional, Tarabykin, Victor, additional, Matsuo, Isao, additional, and Okada, Norihiro, additional

Published
2016
Full Text
View/download PDF

30. Regulation of Otx2 expression and its functions in mouse epiblast and anterior neuroectoderm.

Author

Kurokawa, Daisuke, Takasaki, Nobuyoshi, Kiyonari, Hiroshi, Nakayama, Rika, Kimura-Yoshida, Chiharu, Matsuo, Isao, and Aizawa, Shinichi

Subjects
GENE expression, GENETIC regulation, BRAIN, DIENCEPHALON, XENOPUS
Abstract

We have identified cis-regulatory sequences acting on Otx2 expression in epiblast (EP) and anterior neuroectoderm (AN) at about 90 kb 5′ upstream. The activity of the EP enhancer is found in the inner cell mass at E3.5 and the entire epiblast at E5.5. The AN enhancer activity is detected initially at E7.0 and ceases by E8.5; it is found later in the dorsomedial aspect of the telencephalon at E10.5. The EP enhancer includes multiple nrequired domains over 2.3 kb, and the AN enhancer is an essential component of the EP enhancer. Mutants lacking the AN enhancer have demonstrated that these cis-sequences indeed regulate Otx2 expression in EP and AN. At the same time, our analysis indicates that another EP and AN enhancer must exist outside of the -170 kb to +120 kb range. In Otx2ΔAN/- mutants, in which one Otx2 allele lacks the AN enhancer and the other allele is null, anteroposterior axis forms normally and anterior neuroectoderm is normally induced. Subsequently, however, forebrain and midbrain are lost, indicating that Otx2 expression under the AN enhancer functions to maintain anterior neuroectoderm once induced. Furthermore, Otx2 under the AN enhancer cooperates with Emx2 in diencephalon development. The AN enhancer region is conserved among mouse, human and Xenopus; moreover, the counterpart region in Xenopus exhibited an enhancer activity in mouse anterior neuroectoderm. [ABSTRACT FROM AUTHOR]

Published
2004
Full Text
View/download PDF

31. Genetic modifiers of otocephalic phenotypes in Otx2 heterozygous mutant mice

Author

Hide, Takuichiro, Hatakeyama, Jun, Kimura-Yoshida, Chiharu, Tian, E, Takeda, Naoki, Ushio, Yukitaka, Shiroishi, Toshihiko, Aizawa, Shinichi, and Matsuo, Isao

Abstract

Mice heterozygous for the Otx2 mutation display a craniofacial malformation, known as otocephaly or agnathia-holoprosencephaly complex. The severity of the phenotype is dependent on the genetic background of a C57BL/6 (B6) strain; most of the offspring of Otx2 knock-out chimeras, which are equivalent to the F1 of CBA and B6 strains, backcrossed with B6 females display reduction or loss of mandible, whereas those backcrossed with CBA females do not show noticeable phenotype at birth. The availability of phenotypically disparate strains renders identification of Otx2 modifier loci possible. In this study, a backcross of chimera with B6 was generated and genome-wide scans were conducted with polymorphic markers for non-mendelian distribution of alleles in Otx2 heterozygous mutant mice displaying abnormalities in the lower jaw. We identified one significant locus, Otmf18, between D18Mit68 and D18Mit120 on chromosomes 18, linked to the mandibular phenotype (LOD score 3.33). A similar replication experiment using a second backcross (N3) mouse demonstrated the presence of another significant locus, Otmf2 between D2Mit164 and D2Mit282 on chromosome 2, linked to the mandibular phenotype (LOD score 3.93). These two modifiers account for the distribution of the craniofacial malformations by the genetic effect between B6 and CBA strains. Moreover, Otmf2 contain a candidate gene for several diseases in mice and humans. These genetic studies involving an otocephalic mouse model appear to provide new insights into mechanistic pathways of craniofacial development. Furthermore, these experiments offer a powerful approach with respect to identification and characterization of candidate genes that may contribute to human agnathia-holoprosencephaly complex diseases.

Published
2002
Full Text
View/download PDF

32. Identification of Cell Autonomous and Non-Cell Autonomous Functions of Heparan Sulfate Glycosaminoglycan Chains by Creating Chimeric Mouse Embryos.

Author

Matsuo I and Kimura-Yoshida C

Subjects
Animals, Cell Membrane, Embryo, Mammalian, Heparan Sulfate Proteoglycans, Heparitin Sulfate, Mice, Glycosaminoglycans chemistry
Abstract

Cell surface-tethered heparan sulfate glycosaminoglycan chains primarily function in a cell autonomous manner, while extracellular matrix-associated heparan sulfate glycosaminoglycan chains function in a non-cell autonomous manner. In addition, the cleaved forms of cell surface-tethered heparan sulfate chains enzymatically released by proteases and heparanases, called shedding, can contribute to non-cell autonomous mechanisms. The movement of heparan sulfate chains to surrounding cells mediated by transcytosis or filopodia also involves another non-cell autonomous mechanism. To determine cell autonomous or non-cell autonomous roles of heparan sulfate glycosaminoglycan chains during early embryogenesis, direct conclusions can be drawn by analyzing chimeric embryos which are composed of wild-type and heparan sulfate glycosaminoglycan chain-deficient cells. Here, we describe methods of production of these chimeric embryos and analysis of their cellular phenotypes with immunohistochemistry at a single-cell level., (© 2022. Springer Science+Business Media, LLC, part of Springer Nature.)

Published
2022
Full Text
View/download PDF

33. Extracellular distribution of diffusible growth factors controlled by heparan sulfate proteoglycans during mammalian embryogenesis.

Author

Matsuo I and Kimura-Yoshida C

Subjects
Animals, Biological Transport physiology, Heparan Sulfate Proteoglycans biosynthesis, Heparan Sulfate Proteoglycans chemistry, Mice, Models, Biological, Embryonic Development physiology, Extracellular Space metabolism, Heparan Sulfate Proteoglycans metabolism, Intercellular Signaling Peptides and Proteins metabolism, Signal Transduction physiology
Abstract

During mouse embryogenesis, diffusible growth factors, i.e. fibroblast growth factors, Wnt, bone morphogenetic protein and Hedgehog family members, emanating from localized areas can travel through the extracellular space and reach their target cells to specify the cell fate and form tissue architectures in coordination. However, the mechanisms by which these growth factors travel great distances to their target cells and control the signalling activity as morphogens remain an enigma. Recent studies in mice and other model animals have revealed that heparan sulfate proteoglycans (HSPGs) located on the cell surface (e.g. syndecans and glypicans) and in the extracellular matrix (ECM; e.g. perlecan and agrin) play crucial roles in the extracellular distribution of growth factors. Principally, the function of HSPGs depends primarily on the fine features and localization of their heparan sulfate glycosaminoglycan chains. Cell-surface-tethered HSPGs retain growth factors as co-receptors and/or endocytosis mediators, and enzymatic release of HSPGs from the cell membrane allows HSPGs to transport or move multiple growth factors. By contrast, ECM-associated HSPGs function as a reservoir or barrier in a context-dependent manner. This review is focused on our current understanding of the extracellular distribution of multiple growth factors controlled by HSPGs in mammalian development., (© 2014 The Author(s) Published by the Royal Society. All rights reserved.)

Published
2014
Full Text
View/download PDF

34. [Genetic mechanisms of mouse anterior-posterior patterning].

Author

Matsuo I and Kimura-Yoshida C

Subjects
Animals, Genes, Homeobox, Homeodomain Proteins genetics, Mice, Otx Transcription Factors, Signal Transduction genetics, Signal Transduction physiology, Body Patterning genetics, Homeodomain Proteins physiology
Published
2005

Catalog

Books, media, physical & digital resources
See catalog results