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      Aneuploidy and Genetic Variation in the Arabidopsis thaliana Triploid Response

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      Genetics
      Genetics Society of America

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          Abstract

          Polyploidy, the inheritance of more than two genome copies per cell, has played a major role in the evolution of higher plants. Little is known about the transition from diploidy to polyploidy but in some species, triploids are thought to function as intermediates in this transition. In contrast, in other species triploidy is viewed as a block. We investigated the responses of Arabidopsis thaliana to triploidy. The role of genetic variability was tested by comparing triploids generated from crosses between Col-0, a diploid, and either a natural autotetraploid (Wa-1) or an induced tetraploid of Col-0. In this study, we demonstrate that triploids of A. thaliana are fertile, producing a swarm of different aneuploids. Propagation of the progeny of a triploid for a few generations resulted in diploid and tetraploid cohorts. This demonstrated that, in A. thaliana, triploids can readily form tetraploids and function as bridges between euploid types. Genetic analysis of recombinant inbred lines produced from a triploid identified a locus on chromosome I exhibiting allelic bias in the tetraploid lines but not in the diploid lines. Thus, genetic variation was subject to selection contingent on the final ploidy and possibly acting during the protracted aneuploid phase.

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          Dosage-dependent gene regulation in multicellular eukaryotes: implications for dosage compensation, aneuploid syndromes, and quantitative traits.

          Evidence from a variety of data suggests that regulatory mechanisms in multicellular eukaryotes have evolved in such a manner that the stoichiometric relationship of the components of regulatory complexes affects target gene expression. This type of mechanism sets the level of gene expression and, as a consequence, the phenotypic characteristics. Because many types of regulatory processes exhibit dosage-dependent behavior, they would impact quantitative traits and contribute to their multigenic control in a semidominant fashion. Many dosage-dependent effects would also account for the extensive modulation of gene expression throughout the genome that occurs when chromosomes are added to or subtracted from the karyotype (aneuploidy). Moreover, because the majority of dosage-dependent regulators act negatively, this property can account for the up-regulation of genes in monosomics and hemizygous sex chromosomes to achieve dosage compensation. Copyright 2001 Academic Press.
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            Meiotic pairing and imprinted X chromatin assembly in Caenorhabditis elegans.

            The genetic imprinting of individual loci or whole chromosomes, as in imprinted X-chromosome inactivation in mammals, is established and reset during gametogenesis; defects in this process in the parent can result in disease in the offspring. We describe a sperm-specific chromatin-based imprinting of the X chromosome in the nematode Caenorhabditis elegans that is restricted to histone H3 modifications. The epigenetic imprint is established during spermatogenesis and its stability in the offspring is affected by the presence of a pairing partner during meiosis in the parental germ line. We observed that DNA lacking a pairing partner during meiosis, the normal situation for the X chromosome in males, is targeted for methylation of histone H3 at Lys9 (H3-Lys9) and can be silenced. Targeting unpaired DNA for silencing during meiosis, a potential hallmark of genome defense, could therefore have a conserved role in imprinted X-chromosome inactivation and, ultimately, in sex chromosome evolution.
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              The Origin of Variations in Sexual and Sex-Limited Characters

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                Author and article information

                Journal
                Genetics
                Genetics
                Genetics Society of America
                0016-6731
                1943-2631
                September 06 2005
                August 2005
                August 2005
                June 08 2005
                : 170
                : 4
                : 1979-1988
                Article
                10.1534/genetics.104.037788
                1449780
                15944363
                a3a65c6c-cfca-4390-9a50-d45f6c804576
                © 2005
                History

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