barcode reader vb.net source code Uncovering Plasmids in Software

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How do we know when the phenotype is controlled by a plasmid rather than by the chromosomal genes of a bacterium Plasmids can be seen with an electron microscope or by density-gradient centrifugation of the cell s DNA. But several less direct lines of evidence also supply the answer. To begin with, multiple aspects of the phenotype (e.g., resistance to several antibacterial agents) change simultaneously, as with plasmid R222. Another clue is that the phenotypic change is infectious: Japanese workers found that with R222, resistant cells converted nonresistant cells. As B. Lewin stated, Resistance is infectious. Several other clues point to the presence of a plasmid. In linkage studies, using transduction for example,
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Tamarin: Principles of Genetics, Seventh Edition
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III. Molecular Genetics
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17. Non Mendelian Inheritance
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plasmid loci show no linkage to host loci; plasmids themselves can be mapped because their loci are linked to each other. Since the plasmid DNA replicates at its own speed, it can miss being incorporated into a daughter cell.Thus, many spontaneous losses of the plasmid occur. And nally, certain treatments with acridine dyes, for example have little effect on the replication of the host chromosome, but selectively prevent the plasmid from replicating; thus the plasmid can be eliminated from the cell population. The existence of plasmids in a bacterial population can, therefore, be veri ed with morphological, physiological, and analytical evidence.
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Although sex linkage alters inheritance patterns, we do not expect different inheritance patterns, dependent on the parent of origin, from genes located on autosomal chromosomes. That is, the genotype of an offspring should be predicted by its alleles regardless of which parent donated which allele. That understanding has now been shown to be incorrect for a group of genes whose phenotypic effects are determined by the parent that donated a particular allele. This phenomenon is called imprinting (or molecular imprinting or parental imprinting). It falls under the general classi cation of an epigenetic effect, a term that has come to mean an effect due to an environmentally induced change in the genetic material but not causing a change in base pairs. It is a phenomenon of differential expression of the alleles at a locus depending on which parent the gene originated with. A striking example of imprinting in human beings involves two medical syndromes, both resulting in mental retardation. In Prader-Willi syndrome, affected persons are extremely obese; in Angelman syndrome, those affected are thin and sometimes referred to as happy puppets, because they exhibit a happy facial expression and erratic, jerky movements. It turns out that both syndromes are associated with deletions in the long arm of
chromosome 15, in bands 15q11 q13. The effect is seen in an individual arising from a gamete missing a 15q11 q13 region. If the remaining region is of paternal origin, due to a deletion of the maternal gene, the offspring will have Angelman syndrome; if the remaining region is of maternal origin, the offspring will have PraderWilli syndrome. This unusual situation indicates that the phenotype is dependent on the parent from which the region comes. Recently, this region of chromosome 15 has come under intense scrutiny. In males, from ve to seven genes are expressed from this area, and in females, one gene has been identi ed as the cause of Angelman syndrome, UBE3A (E3 ubiquitin protein ligase). It has been hypothesized that there is an imprinting center (IC), a region responsible for the control of imprinting. The imprinting mark is almost certainly DNA methylation, which has the property of turning off gene transcription. Stretches of CG repeats (called CpG islands, in which CpG indicates sequential bases on the same strand of DNA rather than a C-G base pair) have been found in these imprinting centers. The imprinting center would be the site of the erasure of past imprinting and the initiation of new imprinting during gametogenesis. Over twenty genes exhibit imprinting, and the epigenetic phenomenon also appears in proteins, with differential acetylation of proteins as the imprinting mark. The question arises as to how imprinting evolved; that is, what evolutionary advantages come from silencing an allele from one of the parents Although we don t really know at this point, several hypotheses have been suggested, including competition among maternal and paternal alleles for expression (see chapter 21). For example, the Igf-2 gene (insulin-like growth factor) places demands on pregnant females to produce larger fetuses. This is advantageous to the father (assuming that the female will have offspring from several fathers), but not the mother. So, the mother s gene is usually methylated and therefore inactive. It is as if the genes are in competition with each other, with the father s gene promoting the formation of a large fetus and the mother s gene promoting the formation of a smaller fetus. Currently, the phenomenon of imprinting is under active study.
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