Bioarchitecture最新文献_第8页

Vacuoles in mammals: a subcellular structure indispensable for early embryogenesis. 哺乳动物的液泡:早期胚胎发生不可缺少的亚细胞结构。

Bioarchitecture Pub Date : 2013-01-01 DOI: 10.4161/bioa.24126

Yoh Wada

引用次数: 18

Welcome to BioArchitecture 2013 欢迎来到BioArchitecture 2013

Bioarchitecture Pub Date : 2013-01-01 DOI: 10.4161/BIOA.24027

P. Gunning

引用次数: 1

Spatiotemporal regulation of meiotic recombination by Liaisonin. 连络素对减数分裂重组的时空调控。

Bioarchitecture Pub Date : 2013-01-01 DOI: 10.4161/bioa.23966

Tomoichiro Miyoshi, Masaru Ito, Kunihiro Ohta

{"title":"Spatiotemporal regulation of meiotic recombination by Liaisonin.","authors":"Tomoichiro Miyoshi, Masaru Ito, Kunihiro Ohta","doi":"10.4161/bioa.23966","DOIUrl":"https://doi.org/10.4161/bioa.23966","url":null,"abstract":"Sexual reproduction involves diversification of genetic information in successive generations. Meiotic recombination, which substantially contributes to the increase in genetic diversity, is initiated by programmed DNA double-strand breaks (DSBs) catalyzed by the evolutionarily conserved Spo11 protein. Spo11 requires additional partner proteins for its DNA cleavage reaction. DSBs are preferentially introduced at defined chromosomal sites called \"recombination hotspots.\" Recent studies have revealed that meiotically established higher-order chromosome structures, such as chromosome axes and loops, are also crucial in the control of DSB formation. Most of the DSB sites are located within chromatin loop regions, while many of the proteins involved in DSB formation reside on chromosomal axes. Hence, DSB proteins and DSB sites seem to be distantly located. To resolve this paradox, we conducted comprehensive proteomics and ChIP-chip analyses on Spo11 partners in Schizosaccharomyces pombe, in combination with mutant studies. We identified two distinct DSB complexes, the \"DSBC (DSB Catalytic core)\" and \"SFT (Seven-Fifteen-Twenty four; Rec7-Rec15-Rec24)\" subcomplexes. The DSBC subcomplex contains Spo11 and functions as the catalytic core for the DNA cleavage reaction. The SFT subcomplex is assumed to execute regulatory functions. To activate the DSBC subcomplex, the SFT subcomplex tethers hotspots to axes via its interaction with Mde2, which can interact with proteins in both DSBC and SFT subcomplexes. Thus, Mde2 is likely to bridge these two subcomplexes, forming a \"tethered loop-axis complex.\" It should be noted that Mde2 expression is strictly regulated by S phase checkpoint monitoring of the completion of DNA replication. From these observations, we proposed that Mde2 is a central coupler for meiotic recombination initiation to establish a tethered loop-axis complex in liaison with the S phase checkpoint.","PeriodicalId":89329,"journal":{"name":"Bioarchitecture","volume":"3 1","pages":"20-4"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/bioa.23966","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31347459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12

Akirin: a context-dependent link between transcription and chromatin remodeling. Akirin:转录和染色质重塑之间的上下文依赖联系。

Bioarchitecture Pub Date : 2012-11-01 DOI: 10.4161/bioa.22907

Scott J Nowak, Mary K Baylies

{"title":"Akirin: a context-dependent link between transcription and chromatin remodeling.","authors":"Scott J Nowak, Mary K Baylies","doi":"10.4161/bioa.22907","DOIUrl":"https://doi.org/10.4161/bioa.22907","url":null,"abstract":"Embryonic patterning relies upon an exquisitely timed program of gene regulation. While the regulation of this process via the action of transcription factor networks is well understood, new lines of study have highlighted the importance of a concurrently regulated program of chromatin remodeling during development. Chromatin remodeling refers to the manipulation of the chromatin architecture through rearrangement, repositioning, or restructuring of nucleosomes to either favor or hinder the expression of associated genes. While the role of chromatin remodeling pathways during tumor development and cancer progression are beginning to be clarified, the roles of these pathways in the course of tissue specification, morphogenesis and patterning remains relatively unknown. Further, relatively little is understood as to the mechanism whereby developmentally critical transcription factors coordinate with chromatin remodeling factors to optimize target gene loci for gene expression. Such a mechanism might involve direct transcription factor/chromatin remodeling factor interactions, or could likely be mediated via an unknown intermediary. Our group has identified the relatively unknown protein Akirin as a putative member of this latter group: a secondary cofactor that serves as an interface between a developmentally critical transcription factor and the chromatin remodeling machinery. This role for the Akirin protein suggests a novel regulatory mode for regulating gene expression during development.","PeriodicalId":89329,"journal":{"name":"Bioarchitecture","volume":"2 6","pages":"209-13"},"PeriodicalIF":0.0,"publicationDate":"2012-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/bioa.22907","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31125707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 17

Fibroblast growth factor receptor 3 regulates microtubule formation and cell surface mechanical properties in the developing organ of Corti. 成纤维细胞生长因子受体3调节Corti发育器官的微管形成和细胞表面力学特性。

Bioarchitecture Pub Date : 2012-11-01 DOI: 10.4161/bioa.22332

Katherine B Szarama, Ruben Stepanyan, Ronald S Petralia, Nuria Gavara, Gregory I Frolenkov, Matthew W Kelley, Richard S Chadwick

{"title":"Fibroblast growth factor receptor 3 regulates microtubule formation and cell surface mechanical properties in the developing organ of Corti.","authors":"Katherine B Szarama, Ruben Stepanyan, Ronald S Petralia, Nuria Gavara, Gregory I Frolenkov, Matthew W Kelley, Richard S Chadwick","doi":"10.4161/bioa.22332","DOIUrl":"https://doi.org/10.4161/bioa.22332","url":null,"abstract":"Fibroblast Growth Factor (Fgf) signaling is involved in the exquisite cellular patterning of the developing cochlea, and is necessary for proper hearing function. Our previous data indicate that Fgf signaling disrupts actin, which impacts the surface stiffness of sensory outer hair cells (OHCs) and non-sensory supporting pillar cells (PCs) in the organ of Corti. Here, we used Atomic Force Microscopy (AFM) to measure the impact of loss of function of Fgf-receptor 3, on cytoskeletal formation and cell surface mechanical properties. We find a 50% decrease in both OHC and PC surface stiffness, and a substantial disruption in microtubule formation in PCs. Moreover, we find no change in OHC electromotility of Fgfr3-deficient mice. To further understand the regulation by Fgf-signaling on microtubule formation, we treated wild-type cochlear explants with Fgf-receptor agonist Fgf2, or antagonist SU5402, and find that both treatments lead to a significant reduction in β-Tubulin isotypes I&II. To identify downstream transcriptional targets of Fgf-signaling, we used QPCR arrays to probe 84 cytoskeletal regulators. Of the 5 genes significantly upregulated following treatment, Clasp2, Mapre2 and Mark2 impact microtubule formation. We conclude that microtubule formation is a major downstream effector of Fgf-receptor 3, and suggest this pathway impacts the formation of fluid spaces in the organ of Corti.","PeriodicalId":89329,"journal":{"name":"Bioarchitecture","volume":"2 6","pages":"214-9"},"PeriodicalIF":0.0,"publicationDate":"2012-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/bioa.22332","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31146816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 14

BioArchitecture: the organization and regulation of biological space. 生物建筑:生物空间的组织和调节。

Bioarchitecture Pub Date : 2012-11-01 DOI: 10.4161/bioa.22726

Peter Gunning

引用次数: 1

Sizing up long non-coding RNAs: do lncRNAs have secondary and tertiary structure? 长链非编码rna的分级:lncrna有二级和三级结构吗?

Bioarchitecture Pub Date : 2012-11-01 DOI: 10.4161/bioa.22592

Irina V Novikova, Scott P Hennelly, Karissa Y Sanbonmatsu

引用次数: 128

Microtubule dynamics regulation contributes to endothelial morphogenesis. 微管动力学调控有助于内皮细胞的形态发生。

Bioarchitecture Pub Date : 2012-11-01 DOI: 10.4161/bioa.22335

Karen S Lyle, Jose A Corleto, Torsten Wittmann

引用次数: 1

The role of the cofilin-actin rod stress response in neurodegenerative diseases uncovers potential new drug targets. cofilin-actin棒应激反应在神经退行性疾病中的作用揭示了潜在的新药物靶点。

Bioarchitecture Pub Date : 2012-11-01 DOI: 10.4161/bioa.22549

Lise N Munsie, Ray Truant

{"title":"The role of the cofilin-actin rod stress response in neurodegenerative diseases uncovers potential new drug targets.","authors":"Lise N Munsie, Ray Truant","doi":"10.4161/bioa.22549","DOIUrl":"https://doi.org/10.4161/bioa.22549","url":null,"abstract":"The cofilin-actin rod stress response is an actin cytoskeletal dynamic arrest that occurs in cells under a variety of stress conditions. Upon stress, the rapidly activated cofilin saturates actin filaments causing them to bundle into rod structures in either the nucleus or cytoplasm, halting actin polymerization and thus freeing ATP. Importantly, these rods dissociate quickly following relief of the transient stress. The rods form inappropriately in neurons involved in the progression of Alzheimer disease (AD) and we have linked dysfunctional dynamics of the nuclear rod response to Huntington disease (HD). Cofilin levels are also perturbed in Parkinson disease (PD), and profilin, an actin binding protein with opposite action to cofilin, is mutated in Amyotrophic Lateral Sclerosis (ALS). The persistence of the rods post-stress suggests that critical molecular switches to turn this response both on and off are being affected in neurodegeneration. We have recently shown that the cofilin protein is regulated by highly conserved nuclear import and export signals and that these signals are required to be functional for an appropriate rod formation during stress. The ability of cofilin to form rods is required in a cell culture model for cells to be resistant to apoptosis under stress conditions, indicating that a normal cofilin-actin rod response is likely integral to proper cell health in higher order organisms. Here we hypothesize on the potential physiological function of nuclear cofilin-actin rods and why the dysregulation of this response could lead to the selective vulnerability of the most susceptible populations of cells in HD. We further suggest that learning more about this cytoskeletal cell stress response will open up new avenues for drug target discovery in neurodegenerative disorders.","PeriodicalId":89329,"journal":{"name":"Bioarchitecture","volume":"2 6","pages":"204-8"},"PeriodicalIF":0.0,"publicationDate":"2012-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/bioa.22549","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31146815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 44

Competition and compensation: dissecting the biophysical and functional differences between the class 3 myosin paralogs, myosins 3a and 3b. 竞争和补偿:剖析3类肌球蛋白、3a和3b类肌球蛋白的生物物理和功能差异。

Bioarchitecture Pub Date : 2012-09-01 DOI: 10.4161/bioa.21733

Uri Manor, M'hamed Grati, Christopher M Yengo, Bechara Kachar, Nir S Gov

引用次数: 10