AIMS Genetics最新文献_第8页

AIMS Genetics Pub Date : 2015-01-27 DOI: 10.3934/genet.2015.1.25

M. Murray

引用次数: 6

Cell proliferation control by Notch signalling during imaginal discs development in Drosophila Notch信号在果蝇成像盘发育过程中的细胞增殖调控

AIMS Genetics Pub Date : 2015-01-25 DOI: 10.3934/genet.2015.1.70

Carlos Estella, A. Baonza

引用次数: 7

Neural stem cell derived tumourigenesis 神经干细胞衍生的肿瘤发生

AIMS Genetics Pub Date : 2015-01-11 DOI: 10.3934/genet.2015.1.13

Francesca Froldi, M. Szuperak, Louise Y. Cheng

引用次数: 1

Non-autonomous consequences of cell death and other perks of being metazoan. 细胞死亡的非自主后果和后生动物的其他好处。

AIMS Genetics Pub Date : 2015-01-01 DOI: 10.3934/genet.2015.1.54#sthash.dNy9tFhS.dpuf

Tin Tin Su

引用次数: 10

Drosophila as a model for chromosomal instability 果蝇作为染色体不稳定性的模型

AIMS Genetics Pub Date : 2014-12-16 DOI: 10.3934/genet.2015.1.1

Dawei Liu, Zeeshan Shaukat, R. Hussain, M. Khan, S. Gregory

引用次数: 3

Context-dependent interplay between Hippo and JNK pathway in Drosophila 果蝇Hippo和JNK通路的上下文依赖性相互作用

AIMS Genetics Pub Date : 2014-05-01 DOI: 10.3934/genet.2014.1.20

Xianjue Ma

引用次数: 5

MYC function and regulation in flies: how Drosophila has enlightened MYC cancer biology 果蝇MYC的功能和调控:果蝇如何启发MYC癌症生物学

AIMS Genetics Pub Date : 2014-05-01 DOI: 10.3934/genet.2014.1.81

J. Lee, L. Parsons, L. Quinn

{"title":"MYC function and regulation in flies: how Drosophila has enlightened MYC cancer biology","authors":"J. Lee, L. Parsons, L. Quinn","doi":"10.3934/genet.2014.1.81","DOIUrl":"https://doi.org/10.3934/genet.2014.1.81","url":null,"abstract":"Abstract Progress in our understanding of the complex signaling events driving human cancer would have been unimaginably slow without discoveries from Drosophila genetic studies. Significantly, many of the signaling pathways now synonymous with cancer biology were first identified as a result of elegant screens for genes fundamental to metazoan development. Indeed the name given to many core cancer-signaling cascades tells of their history as developmental patterning regulators in flies—e.g. Wingless (Wnt), Notch and Hippo. Moreover, astonishing insight has been gained into these complex signaling networks, and many other classic oncogenic signaling networks (e.g. EGFR/RAS/RAF/ERK, InR/PI3K/AKT/TOR), using sophisticated fly genetics. Of course if we are to understand how these signaling pathways drive cancer, we must determine the downstream program(s) of gene expression activated to promote the cell and tissue over growth fundamental to cancer. Here we discuss one commonality between each of these pathways: they are all implicated as upstream activators of the highly conserved MYC oncogene and transcription factor. MYC can drive all aspects of cell growth and cell cycle progression during animal development. MYC is estimated to be dysregulated in over 50% of all cancers, underscoring the importance of elucidating the signals activating MYC. We also discuss the FUBP1/FIR/FUSE system, which acts as a ‘cruise control’ on the MYC promoter to control RNA Polymerase II pausing and, therefore, MYC transcription in response to the developmental signaling environment. Importantly, the striking conservation between humans and flies within these major axes of MYC regulation has made Drosophila an extremely valuable model organism for cancer research. We therefore discuss how Drosophila studies have helped determine the validity of signaling pathways regulating MYC in vivo using sophisticated genetics, and continue to provide novel insight into cancer biology.","PeriodicalId":43477,"journal":{"name":"AIMS Genetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70248440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10

The Drosophila gonads: models for stem cell proliferation, self-renewal, and differentiation 果蝇性腺:干细胞增殖、自我更新和分化的模型

AIMS Genetics Pub Date : 2014-05-01 DOI: 10.3934/genet.2014.1.55

J. Marca, W. G. Somers

引用次数: 3

Comparative epigenomics: an emerging field with breakthrough potential to understand evolution of epigenetic regulation 比较表观基因组学:理解表观遗传调控进化的一个具有突破性潜力的新兴领域

AIMS Genetics Pub Date : 2014-05-01 DOI: 10.3934/genet.2014.1.34

J. Deakin, R. Domaschenz, P. S. Lim, T. Ezaz, Sudha Rao

{"title":"Comparative epigenomics: an emerging field with breakthrough potential to understand evolution of epigenetic regulation","authors":"J. Deakin, R. Domaschenz, P. S. Lim, T. Ezaz, Sudha Rao","doi":"10.3934/genet.2014.1.34","DOIUrl":"https://doi.org/10.3934/genet.2014.1.34","url":null,"abstract":"Abstract Epigenetic mechanisms regulate gene expression, thereby mediating the interaction between environment, genotype and phenotype. Changes to epigenetic regulation of genes may be heritable, permitting rapid adaptation of a species to environmental cues. However, most of the current understanding of epigenetic gene regulation has been gained from studies of mice and humans, with only a limited understanding of the conservation of epigenetic mechanisms across divergent taxa. The relative ease at which genome sequence data is now obtained and the advancements made in epigenomics techniques for non-model species provides a basis for carrying out comparative epigenomic studies across a wider range of species, making it possible to start unraveling the evolution of epigenetic mechanisms. We review the current knowledge of epigenetic mechanisms obtained from studying model organisms, give an example of how comparative epigenomics using non-model species is helping to trace the evolutionary history of X chromosome inactivation in mammals and explore the opportunities to study comparative epigenomics in biological systems displaying adaptation between species, such as the immune system and sex determination.","PeriodicalId":43477,"journal":{"name":"AIMS Genetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70248384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Allelic Interaction between CRELD1 and VEGFA in the Pathogenesis of Cardiac Atrioventricular Septal Defects CRELD1和VEGFA等位基因在心脏房室间隔缺损发病机制中的相互作用

AIMS Genetics Pub Date : 2014-03-11 DOI: 10.3934/genet.2014.1.1

Jennifer K Redig, G. Fouad, D. Babcock, Benjamin Reshey, E. Feingold, R. Reeves, C. Maslen

{"title":"Allelic Interaction between CRELD1 and VEGFA in the Pathogenesis of Cardiac Atrioventricular Septal Defects","authors":"Jennifer K Redig, G. Fouad, D. Babcock, Benjamin Reshey, E. Feingold, R. Reeves, C. Maslen","doi":"10.3934/genet.2014.1.1","DOIUrl":"https://doi.org/10.3934/genet.2014.1.1","url":null,"abstract":"Abstract Atrioventricular septal defects (AVSD) are highly heritable, clinically significant congenital heart malformations. Genetic and environmental modifiers of risk are thought to work in unknown combinations to cause AVSD. Approximately 5–10% of simplex AVSD cases carry a missense mutation in CRELD1. However, CRELD1 mutations are not fully penetrant and require interactions with other risk factors to result in AVSD. Vascular endothelial growth factor-A (VEGFA) is a well-characterized modulator of heart valve development. A functional VEGFA polymorphism, VEGFA c.−634C, which causes constitutively increased VEGFA expression, has been associated with cardiac septal defects suggesting it may be a genetic risk factor. To determine if there is an allelic association with AVSD we genotyped the VEGFA c.−634 SNP in a simplex AVSD study cohort. Over-representation of the c.−634C allele in the AVSD group suggested that this genotype may increase risk. Correlation of CRELD1 and VEGFA genotypes revealed that potentially pathogenic missense mutations in CRELD1 were always accompanied by the VEGFA c.−634C allele in individuals with AVSD suggesting a potentially pathogenic allelic interaction. We used a Creld1 knockout mouse model to determine the effect of deficiency of Creld1 combined with increased VEGFA on atrioventricular canal development. Morphogenic response to VEGFA was abnormal in Creld1-deficient embryonic hearts, indicating that interaction between CRELD1 and VEGFA has the potential to alter atrioventricular canal morphogenesis. This supports our hypothesis that an additive effect between missense mutations in CRELD1 and a functional SNP in VEGFA contributes to the pathogenesis of AVSD.","PeriodicalId":43477,"journal":{"name":"AIMS Genetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2014-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70248309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12