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Genetic Redundancy (genetic + redundancy)
Selected AbstractsGenetic redundancy in human cervical carcinoma cells: Identification of cells with "normal" propertiesINTERNATIONAL JOURNAL OF CANCER, Issue 10 2007Anastasia Bachmann Abstract Although it is generally assumed that cancer arises from a singular cell, a tumor must be considered as a dynamic and emergent biological structure, whose organizing principle is determined by genetic and epigenetic modifications, occurring variably in response to microenvironmental selection conditions. As previously shown, HPV-positive cervical carcinoma cells have lost their ability to induce IFN-, upon TNF-, treatment. However, regarding cancer as a non-linear system, which may, even in the absence of an apparent selection pressure, fluctuate between different "metastable" phenotypes, we demonstrate that TNF-, mediated IFN-, induction is not irreversibly disturbed in all cells. Using the IFN-, sensitive Encephalomyocarditis virus (EMCV) as a tool to monitor antiviral activity in long-term established malignant HeLa cells, rare IFN-, expressing clones were rescued from a population of non-responsive and EMCV-sensitive cells. Antiviral activity was mediated by the re-expression of IRF-1 and p48 (IRF-9), both key regulatory molecules normally found to be suppressed in cervical carcinoma cells. Upon inoculating of selected clones into immunocompromised animals, a reduced or even an absence of tumorigenicity of initially highly malignant cells could be discerned. These data indicate that both the absence of interferon signaling and the ability to form tumors were reversed in a minority of cells. We provide a paradigm for the existence of innate genetic redundancy mechanisms, where a particular phenotype persists and can be isolated without application of drugs generally changing the epigenetic context. © 2007 Wiley-Liss, Inc. [source] SHORT COMMUNICATION: Response to Dr Stephen Cooper's ,On the use of metaphor to understand, explain, or rationalize redundant genes in yeast'FEMS YEAST RESEARCH, Issue 3 2008Xuewen Pan Abstract Earlier use of a metaphor in explaining genetic redundancy in a news article has triggered a commentary and a competing metaphor by Dr Stephen Cooper, who went on to conclude that genetic redundancies are relatively unimportant for microorganisms. We argue here that the new metaphor is flawed and that genetic redundancies are integral to buffering all organisms against environmental and genetic damage. [source] Sfrp5 is not essential for axis formation in the mouse,GENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 12 2006Irina Leaf Abstract Secreted frizzled related protein (Sfrp) genes encode extracellular factors that can modulate Wnt signaling. During early post-implantation mouse development Sfrp5 is expressed in the anterior visceral endoderm (AVE) and the ventral foregut endoderm. The AVE is important in anterior,posterior axis formation and the ventral foregut endoderm contributes to multiple gut tissues. Here to determine the essential role of Sfrp5 in early mouse development we generated Sfrp5 -deficient mice by gene targeting. We report that Sfrp5 -deficient mice are viable and fertile. To determine whether the absence of an axis phenotype might be due to genetic redundancy with Dkk1 in the AVE we generated Sfrp5;Dkk1 double mutant mice. AVE development and primitive streak formation appeared normal in Sfrp5,/,;Dkk1,/, embryos. These results indicate that Sfrp5 is not essential for axis formation or foregut morphogenesis in the mouse and also imply that Sfrp5 and Dkk1 together are not essential for AVE development. genesis 44:573,578, 2006. Published 2006 Wiley-Liss, Inc. [source] | ||||||||||