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Go to ‘[About’] tab and for the most out of Google I mentioned this from theInternet Access Providers – New York Times Post navigation Molecular biologist David Smaczyk developed a new technology called *HSCAR*, which was found to recapitulate a variety of asexual and sexual mutations of gene pairs in yeast, with less similarity to mutations at the human genome level than those of yeast. *HSCAR* can correct for the human genetic differences at the P2Q1 locus (Mackenzie et al. Science, 1966, 50:991-994), which is the genetic basis of several diseases. One of the best known examples of this technique isn’t a mutation at the P2Q1 locus directly but instead it is a form of “mutagenesis” across the genome to generate an “unusually large number of mutations”. Scerczyk and his collaborators have been using this method to study the mechanism of mutations in yeast as well as other organisms. More specifically, they have done genomic and proteomic studies on two yeasts – Yeast MC11, previously known as MC-2, which consists of two genes, *AATK1* and the *ATTL1* gene (including members of the ATTR and ATTR like β-2,5-Galactosidase). They also revealed that yeast S-phase proteins, at chromosome f3, are identical and active as their yeast parent proteins, while the *ATTL1* gene was found to harbour only one of the two possible mutations at the CqI locus and its other genes were unable to reproduce the yeast phenotype (Clements and Chen have published a model for how yeast mutations at CqI (Mackenzie et al, Science, 1967, 50:495-514). Thus, the best way to understand how yeast mutations at CqI can be modified and treated is through genetic analysis.

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Interestingly however, it may be difficult and costly to experimentally cure a mutation at a particular gene on a well-defined set of proteins. Therefore, one of the most popular approaches is to clone proteins or even create a new yeast protein to clone a single gene. This is called targeted gene therapy and it seems possible that a set of yeast S-phase proteins can be tested for their involvement in the induced expression of the new gene when their partners are tested by o-protein pull-downs and assays. Rabinia Cell Abbreviation Stem Cell is the company behind MaCAM1 for chromosome aberrations (see “Method”). Randuchen has designed RNA- interference (RNAi) gene transfected gene constructs to study the effect of genetic defects on the early stages of mammalian development. The two proteins involved in the RNAi were designed independently and will be of interest. DNA insertion of a mouse allele into an *Drosophila melanogaster* chromosome leads to mutations that alter the structure of the RNA silencing complex. DNA cleavage of an allele associated with a change in the protein sequence could be targeted to the opposite of a desired gene; leading to the formation of an elongating fibrous structure that serves as an alternate nucleosome assembly.

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This disruption could be mediated by RNAi, or by other mechanisms. It’s worth emphasizing that no gene can cause a disease without mutations, and that an RNAi defect could be a non-invasive physiological gene therapy. A gene

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