カテゴリ:[ 子供/学校/教育 ]


[29] 転写因子FoxP2が高等哺乳動物の小細胞性細胞で同定された

投稿者: ほり 投稿日:2016年 6月14日(火)18時43分21秒 133-28-92-222.ptr.kanazawa-u.ac.jp  通報   返信・引用

FoxP2 is a parvocellular-specific transcription factor in the visual thalamus of monkeys and ferrets.

Lena Iwai, Yohei Ohashi, Deborah van der List, William Martin Usrey, Yasushi Miyashita and Hiroshi Kawasaki

Cerebral Cortex (2013, September)

PMID: 22791804



Although the parallel visual pathways are a fundamental basis of visual processing, our knowledge of their molecular properties is still limited. Here, we uncovered a parvocellular-specific molecule in the dorsal lateral geniculate nucleus (dLGN) of higher mammals. We found that FoxP2 transcription factor was specifically expressed in X cells of the adult ferret dLGN. Interestingly, FoxP2 was also specifically expressed in parvocellular layers 3-6 of the dLGN of adult old world monkeys, providing new evidence for a homology between X cells in the ferret dLGN and parvocellular cells in the monkey dLGN. Furthermore, this expression pattern was established as early as gestation day 140 in the embryonic monkey dLGN, suggesting that parvocellular specification has already occurred when the cytoarchitectonic dLGN layers are formed. Our results should help in gaining a fundamental understanding of the development, evolution, and function of the parallel visual pathways, which are especially prominent in higher mammals.

[28] 大脳皮質の形成における転写因子Sox11の役割

投稿者: ほり 投稿日:2016年 6月14日(火)17時47分23秒 133-28-92-222.ptr.kanazawa-u.ac.jp  通報   返信・引用

Sox11 Balances Dendritic Morphogenesis with Neuronal Migration in the Developing Cerebral Cortex.

Yoshio Hoshiba, Tomohisa Toda, Haruka Ebisu, Mayu Wakimoto, Shigeru Yanagi and Hiroshi Kawasaki1,2

The Journal of Neuroscience(2016, May)



神経細胞移動(neural migration)は複雑な神経細胞の配置を可能にし、正しい神経回路を提供するとされています。


The coordinated mechanisms balancing promotion and suppression of dendritic morphogenesis are crucial for the development of the cerebral cortex. Although previous studies have revealed important transcription factors that promote dendritic morphogenesis during development, those that suppress dendritic morphogenesis are still largely unknown. Here we found that the expression levels of the transcription factor Sox11 decreased dramatically during dendritic morphogenesis. Our loss- and gain-of-function studies using postnatal electroporation and in utero electroporation indicate that Sox11 is necessary and sufficient for inhibiting dendritic morphogenesis of excitatory neurons in the mouse cerebral cortex during development. Interestingly, we found that precocious suppression of Sox11 expression caused precocious branching of neurites and a neuronal migration defect. We also found that the end of radial migration induced the reduction of Sox11 expression. These findings indicate that suppression of dendritic morphogenesis by Sox11 during radial migration is crucial for the formation of the cerebral cortex.

[27] 遺伝子に変異が入ったかどうかを確認する方法(CRISPR/Cas9)

投稿者: ほり 投稿日:2016年 6月14日(火)10時01分56秒 133-28-92-222.ptr.kanazawa-u.ac.jp  通報   返信・引用

A Rapid and Cheap Methodology for CRISPR/Cas9 Zebrafish Mutant Screening

Ylenia D’Agostino ? Annamaria Locascio ? Filomena Ristoratore ?Paolo Sordino ? Antonietta Spagnuolo ? Marco Borra ? Salvatore D’Aniello

Mol Biotechnol (2016, Jan)

PMID: 26676479






*結構軽めの論文です←Fig. も一個しかありません


he introduction of new genome editing tools such as ZFNs, TALENs and, more recently, the CRISPR/Cas9 system, has greatly expanded the ability to knock-out genes in different animal models, including zebrafish. However, time and costs required for the screening of a huge number of animals, aimed to identify first founder fishes (F0), and then carriers (F1) are still a bottleneck. Currently, high-resolution melting (HRM) analysis is the most efficient technology for large-scale InDels detection, but the very expensive equipment demanded for its application may represent a limitation for research laboratories. Here, we propose a rapid and cheap method for high-throughput genotyping that displays efficiency rate similar to the HRM. In fact, using a common ViiA™7 real-time PCR system and optimizing the parameters of the melting analysis, we demonstrated that it is possible to discriminate between the mutant and the wild type melting curves. Due to its simplicity, rapidity and cheapness, our method can be used as a preliminary one-step approach for massive screening, in order to restrict the scope at a limited number of embryos and to focus merely on them for the next sequencing step, necessary for the exact sequence identification of the induced mutation. Moreover, thanks to its versatility, this simple approach can be readily adapted to the detection of any kind of genome editing approach directed to genes or regulatory regions and can be applied to many other animal models.

[26] 線虫におけるCRISPR/Cas9シズテム

投稿者: ほり 投稿日:2016年 6月14日(火)09時34分59秒 133-28-92-222.ptr.kanazawa-u.ac.jp  通報   返信・引用

Heritable genome editing in C. elegans via a CRISPR-Cas9 system

Ari E Friedland, Yonatan B Tzur, Kevin M Esvelt, Monica P Colaia?covo, George M Church & John A Calarco

nature methods (2013, AUGUST)

PMID: 2381706




We report the use of clustered, regularly interspaced, short palindromic repeats (CRISPR)-associated endonuclease Cas9 to target genomic sequences in the Caenorhabditis elegans germ line using single-guide RNAs that are expressed from a U6 small nuclear RNA promoter. Our results demonstrate that targeted, heritable genetic alterations can be achieved in C. elegans, providing a convenient and effective approach for generating loss-of-function mutants.

[25] これ堀池君から聞いていたっけ?

投稿者: 雪田 投稿日:2016年 5月27日(金)17時08分47秒 gw22.shizuoka.ac.jp  通報   返信・引用

Hum Mol Genet. 2015 Jan 15;24(2):424-35. doi: 10.1093/hmg/ddu458. Epub 2014 Sep 10.

Loss of Tbx1 induces bone phenotypes similar to cleidocranial dysplasia.

Funato N1, Nakamura M2, Richardson JA3, Srivastava D4, Yanagisawa H5.

Author information


T-box transcription factor, TBX1, is the major candidate gene for 22q11.2 deletion syndrome (DiGeorge/ Velo-cardio-facial syndrome) characterized by facial defects, thymus hypoplasia, cardiovascular anomalies and cleft palates. Here, we report that the loss of Tbx1 in mouse (Tbx1(-/-)) results in skeletal abnormalities similar to those of cleidocranial dysplasia (CCD) in humans, which is an autosomal-dominant skeletal disease caused by mutations in RUNX2. Tbx1(-/-) mice display short stature, absence of hyoid bone, failed closure of fontanelle, bifid xiphoid process and hypoplasia of clavicle and zygomatic arch. A cell-type-specific deletion of Tbx1 in osteochondro-progenitor (Tbx1(OPKO)) or mesodermal (Tbx1(MKO)) lineage partially recapitulates the Tbx1(-/-) bone phenotypes. Although Tbx1 expression has not been previously reported in neural crest, inactivation of Tbx1 in the neural crest lineage (Tbx1(NCKO)) leads to an absence of the body of hyoid bone and postnatal lethality, indicating an unanticipated role of Tbx1 in neural crest development. Indeed, Tbx1 is expressed in the neural crest-derived hyoid bone primordium, in addition to mesoderm-derived osteochondral progenitors. Ablation of Tbx1 affected Runx2 expression in calvarial bones and overexpression of Tbx1 induced Runx2 expression in vitro. Taken together, our current studies reveal that Tbx1 is required for mesoderm- and neural crest-derived osteoblast differentiation and normal skeletal development. TBX1 mutation could lead to CCD-like bone phenotypes in human.

[24] ヒトにおいてもTBX19が同定されています

投稿者: ほり 投稿日:2015年12月11日(金)11時54分56秒 gw22.shizuoka.ac.jp  通報   返信・引用   編集済

Identification, Mapping, and Phylogenomic Analysis of Four New Human Members of the T-box Gene Family:EOMES, TBX6, TBX18, and TBX19

Cheong-Ho Yi,* Jonathan A. Terrett,† Quan-Yi Li,† Kathryn Ellington,† Elizabeth A. Packham,* Lindsay Armstrong-Buisseret,* Patrick McClure,* Tim Slingsby,* and J. David Brook*,1

Genomics 55, 10?20 (1999)

PMID: 9888994




遺伝子座については「Hkaea49」「N73939 」などの見慣れない単語ばかり登場するため、
理解しずらいところもありますが、Tbox gene の構造を理解するには良いものなのかなと思います。

Brachyury(T) is a mouse mutation, first described over 70 years ago, that causes defects in mesoderm formation. Recently several related genes, the T-box gene family, that encode a similar N-terminal DNA binding domain, the T-box, and that play critical roles in human embryonic development have been identi- fied. It has been shown that human TBX5 and TBX3, if mutated, cause developmental disorders, Holt?Oram syndrome (OMIM 142900) and ulnar-mammary syn- drome (OMIM 181450), respectively. We have identi- fied four new human members of the T-box gene fam- ily, EOMES, TBX6, TBX18, and TBX19, and these genes have been mapped to different chromosomal regions by radiation hybrid mapping. The four T-box genes were classified into four different subfamilies and have also been subjected to phylogenomic analysis. Human EOMES maps at 3p21.3?p21.2. This Tbr1-sub- family gene is likely to play a significant role in early embryogenesis similar to that described for Xenopus eomesodermin. Human TBX6 maps at 16p12?q12. This Tbx6-subfamily gene is likely to participate in paraxial mesoderm formation and somitogenesis in human em- bryo. TBX18 is a novel member of the Tbx1 subfamily that maps at 6q14?q15. Two subgroups, TBX1/10 and TBX15/18 subgroups, could be distinguished within the Tbx1 subfamily. TBX19 is an orthologue of chick TbxT and maps at 1q23? q24. The genomic organization of TBX19 is highly similar to that of human T(Brachyury), another human member of the same subfamily.

[23] Tbox gene に関するreviewの紹介

投稿者: ほり 投稿日:2015年12月11日(金)11時10分48秒 gw22.shizuoka.ac.jp  通報   返信・引用   編集済


The T-box gene family

Virginia E. Papaioannou* and Lee M. Silver

BioEssays 20:9-19 (1998)

1. Tbox geneがどのようにして発見されたのか
2. 系統学的に見て、Tbox gene familyはどのようなsub familyに分けることができるのか
3. 発生におけてTbox gene が果たす役割


A novel family of transcription factors that appears to play a critical role in the development of all animal species was recently uncovered on the basis of homology to the DNA binding domain of the Brachyury, or T locus, gene product. Phylogenetic studies have shown the ancient origin of this gene family, which has been named the T-box family, prior to the divergence of metazoa from a common ancestral type. T-box genes have now been identified in the genomes of C. elegans, Drosophila, sea urchin, ascidian, amphioxus, Xenopus, chick, zebrafish, mouse, and human and will probably be found in the genomes of all animals. Although functional analyses of T-box family members have just begun, the results show a wide range of roles in developmental processes that extend over time from the unfertilized egg through organogenesis. Only a few mutations in T-box genes are known, but all have drastic effects on development, including a targeted mutation in mice causing an embryonic lethal phenotype, and two human T-box gene mutations that results in developmental syndromes. This review presents a current overview of progress made in the analysis of T-box genes and their products in a variety of model systems. BioEssays 20:9?19, 1998. ? 1998 John Wiley & Sons, Inc.

[21] Tbx4の発現を促すPitx1は後肢の形成に必要である

投稿者: ほり 投稿日:2015年11月 8日(日)07時21分9秒 softbank126080244194.bbtec.net  通報   返信・引用   編集済

Pitx1 is necessary for normal initiation of hindlimb outgrowth through regulation of Tbx4 expression and shapes hindlimb morphologies via targeted growth control

Veronique Duboc and Malcolm P. O. Logan*

Development. 2011 Dec;138(24):5301-9. doi: 10.1242/dev.074153. Epub 2011 Nov 9.

PMID: 22071103





The forelimbs and hindlimbs of vertebrates are morphologically distinct. Pitx1, expressed in the hindlimb bud mesenchyme, is required for the formation of hindlimb characteristics and produces hindlimb-like morphologies when misexpressed in forelimbs. Pitx1 is also necessary for normal expression of Tbx4, a transcription factor required for normal hindlimb development. Despite the importance of this protein in these processes, little is known about its mechanism of action. Using a transgenic gene replacement strategy in a Pitx1 mutant mouse, we have uncoupled two discrete functions of Pitx1. We show that, firstly, this protein influences hindlimb outgrowth by regulating Tbx4 expression levels and that, subsequently, it shapes hindlimb bone and soft tissue morphology independently of Tbx4. We provide the first description of how Pitx1 sculpts the forming hindlimb skeleton by localised modulation of the growth rate of discrete elements.

KEY WORDS: Pitx1, Limb-type morphology, Tbx4, Mouse

[20] Tbx5はマウスの胸骨形成と調節、鳥類の胸骨と前肢の形成に関与している

投稿者: ほり 投稿日:2015年11月 3日(火)12時14分17秒 posmail.toshin.com  通報   返信・引用

PNAS, December 16, 2014, vol. 111, no. 50, 17917-17922
Regulatory modulation of the T-box gene Tbx5 links development, evolution, and adaptation of the sternum
Sorrel R. B. Bickley and Malcolm P. O. Logan

今回はT-box geneのTbx5に関する論文です。




[19] Nogginタンパク質の新たな役割:Activin/NodalとWntシグナル伝達の阻害

投稿者: あさみ 投稿日:2015年10月 8日(木)11時44分11秒 gw22.shizuoka.ac.jp  通報   返信・引用

Development. 2011 Dec;138(24):5345-56. doi: 10.1242/dev.068908. Epub 2011 Nov 9.

PMID: 22071106

Novel functions of Noggin proteins: inhibition of Activin/Nodal and Wnt signaling.


The secreted protein Noggin1 is an embryonic inducer that can sequester TGFβ cytokines of the BMP family with extremely high affinity. Owing to this function, ectopic Noggin1 can induce formation of the headless secondary body axis in Xenopus embryos. Here, we show that Noggin1 and its homolog Noggin2 can also bind, albeit less effectively, to ActivinB, Nodal/Xnrs and XWnt8, inactivation of which, together with BMP, is essential for the head induction. In support of this, we show that both Noggin proteins, if ectopically produced in sufficient concentrations in Xenopus embryo, can induce a secondary head, including the forebrain. During normal development, however, Noggin1 mRNA is translated in the presumptive forebrain with low efficiency, which provides the sufficient protein concentration for only its BMP-antagonizing function. By contrast, Noggin2, which is produced in cells of the anterior margin of the neural plate at a higher concentration, also protects the developing forebrain from inhibition by ActivinB and XWnt8 signaling. Thus, besides revealing of novel functions of Noggin proteins, our findings demonstrate that specification of the forebrain requires isolation of its cells from BMP, Activin/Nodal and Wnt signaling not only during gastrulation but also at post-gastrulation stages.


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