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|Title:||Genome interactions in polyploid plant species : an investigation of poaceae (tribe triticeae)|
|Presented at:||University of Leicester|
|Abstract:||The 120-bp repetitive sequence family, a widespread and old component of Triticeae genomes, has been used as a tool for investigating genome interactions in Triticeae allopolyploids. Changes in copy number of 120-bp repeat unit family were hypothesised to happen as a result of hybridization events generating Triticeae allopolyploids together with increase and decrease in DNA methylation of this major fraction of Triticeae genomes. In addition, by using 120-bp repeat family sequences for identifying chromosomes from different genomes in Triticeae allopolyploids whole-genome DNA methylation patterns were investigated on chromosome spreads. In all Triticeae allopolyploid species investigated in the present work, unevenly distributed whole-genome methylation patterns were present with enhanced and reduced methylation signal in different chromosomes pairs and/or different chromosomal regions, while diploid Triticeae species showed uniformly distributed whole-genome methylation patterns along their chromosomes. The role of repetitive sequences in relocating the overall DNA methylation through local increase and decrease in different chromatin regions and in contributing to coordinate the heterochromatin of different genome donors in a new allopolyploid species was discussed. Finally, two different examples of alteration of methylation patterns have been investigated in Triticale allopolyploids. In the former case, alterations in whole-genome methylation and methylation patterns of two different repetitive DNA fractions, 120-bp repeat unit family and 5S rDNA sequences were observed in the early generations obtained by crossing two advanced Triticale lines but the "memory" of methylation code was quickly re-established with no effect on plant growth. In the latter, treatments with 5-azacytidine, an inhibitor of DNA methylation, greatly reduced but not completely erased from chromosomes the methylation signal..|
|Rights:||Copyright © the author. All rights reserved.|
|Appears in Collections:||Theses, Dept. of Biology|
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