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R. E. Masonbrink, S. Fu, F. Han, and J. A. Birchler. Heritable Loss of Replication Control of a Minichromosome Derived From the B Chromosome of Maize. Genetics. 2013, 193: 77-84.

R. E. Masonbrink, S. Fu, F. Han, and J. A. Birchler. Heritable Loss of Replication Control of a Minichromosome Derived From the B Chromosome of Maize. Genetics. 2013, 193: 77-84.

 

Abstract:During an accumulation regime of a small telomere-truncated B chromosome, a derivative with large variations in size and multiple punctate centromere loci exhibiting amplified copy numbers was discovered. Multiple centromere satellite loci or transgene signals were documented in amplified chromosomes, suggesting over-replication. Immunolocalization studies revealed multiple foci of biochemical markers characteristic of active centromeres such as CENP-C and phosphorylation of histones H3S10 and H2AThr133. The amplified chromosomes exhibit an absence of chromosome disjunction in meiosis I and an infrequent chromosome disjunction in meiosis II. Despite their unusual structure and behavior these chromosomes were observed in the lineage for seven generations during the course of this study. While severely truncated relative to a normal B chromosome, the progenitor minichromosome is estimated to be at least several megabases in size. Given that the centromere and transgene signals at opposite ends of the chromosome generally match in copy number, the replication control is apparently lost over several megabases.

 

文章链接:http://www.ncbi.nlm.nih.gov/pubmed/23114381

 
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