AIMS GeneticsPub Date : 2014-12-16DOI: 10.3934/genet.2015.1.1
Dawei Liu, Zeeshan Shaukat, R. Hussain, M. Khan, S. Gregory
{"title":"Drosophila as a model for chromosomal instability","authors":"Dawei Liu, Zeeshan Shaukat, R. Hussain, M. Khan, S. Gregory","doi":"10.3934/genet.2015.1.1","DOIUrl":"https://doi.org/10.3934/genet.2015.1.1","url":null,"abstract":"Abstract Chromosomal instability (CIN) is a common feature of tumours that leads to increased genetic diversity in the tumour and poor clinical outcomes. There is considerable interest in understanding how CIN comes about and how its contribution to drug resistance and metastasis might be counteracted. In the last decade a number of CIN model systems have been developed in Drosophila that offer unique benefits both in understanding the development of CIN in a live animal as well as giving the potential to do genome wide screens for therapeutic candidate genes. This review outlines the mechanisms used in several Drosophila CIN model systems and summarizes some significant outcomes and opportunities that they have produced.","PeriodicalId":43477,"journal":{"name":"AIMS Genetics","volume":"02 1","pages":"001 - 012"},"PeriodicalIF":0.0,"publicationDate":"2014-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70248490","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}
AIMS GeneticsPub Date : 2014-05-01DOI: 10.3934/genet.2014.1.20
Xianjue Ma
{"title":"Context-dependent interplay between Hippo and JNK pathway in Drosophila","authors":"Xianjue Ma","doi":"10.3934/genet.2014.1.20","DOIUrl":"https://doi.org/10.3934/genet.2014.1.20","url":null,"abstract":"Abstract Both Hippo and JNK signaling have well-established roles in regulating many physiological processes, including cell proliferation, growth, survival, and migration. An increasing body of evidence shows that dysregulation of either Hippo or JNK pathway would lead to tumorigenesis. Recently, studies in Drosophila has coupled Hippo with JNK pathway in numerous ways ranging from tissue regeneration to growth control. In this review, I provide an overview of the current understanding of crosstalk between Hippo and JNK pathway in Drosophila, and discuss their context-dependent interactions in gut homeostasis, regeneration, cell competition and migration.","PeriodicalId":43477,"journal":{"name":"AIMS Genetics","volume":"01 1","pages":"020 - 033"},"PeriodicalIF":0.0,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70248374","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}
AIMS GeneticsPub Date : 2014-05-01DOI: 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":"01 1","pages":"081 - 098"},"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}
AIMS GeneticsPub Date : 2014-05-01DOI: 10.3934/genet.2014.1.55
J. Marca, W. G. Somers
{"title":"The Drosophila gonads: models for stem cell proliferation, self-renewal, and differentiation","authors":"J. Marca, W. G. Somers","doi":"10.3934/genet.2014.1.55","DOIUrl":"https://doi.org/10.3934/genet.2014.1.55","url":null,"abstract":"Abstract The male and female gonads of Drosophila melanogaster have developed into powerful model systems for both the study of stem cell behaviours, and for understanding how stem cell misregulation can lead to cancers. Using these systems, one is able to observe and manipulate the resident stem cell populations in vivo with a great deal of licence. The tractability of the testis and ovary also allow researchers to explore a range of cellular mechanisms, such as proliferation and polarity, as well as the influence exerted by the local environment through a host of highly-conserved signalling pathways. Importantly, many of the cellular behaviours and processes studied in the Drosophila testis and ovary are known to be disrupted, or otherwise misregulated, in human tumourigenic cells. Here, we review the mechanisms relating to stem cell behaviour, though we acknowledge there are many other fascinating aspects of gametogenesis, including the invasive behaviour of migratory border cells in the Drosophila ovary that, though relevant to the study of tumourigenesis, will unfortunately not be covered.","PeriodicalId":43477,"journal":{"name":"AIMS Genetics","volume":"01 1","pages":"055 - 080"},"PeriodicalIF":0.0,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70248428","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}
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