PUBLICATION

The random versus fragile breakage models of chromosome evolution: a matter of resolution

Authors
Becker, T.S., and Lenhard, B.
ID
ZDB-PUB-070920-11
Date
2007
Source
Molecular genetics and genomics : MGG   278(5): 487-491 (Review)
Registered Authors
Becker, Thomas S.
Keywords
Genome evolution, Synteny blocks, Genomic regulatory blocks, Bystander gene
MeSH Terms
  • Animals
  • Chromosome Mapping
  • Chromosomes/ultrastructure*
  • DNA Damage*
  • Evolution, Molecular
  • Genetic Techniques
  • Genome
  • Genomics
  • Humans
  • Models, Biological
  • Models, Genetic
  • Synteny
  • Zebrafish
PubMed
17851692 Full text @ Mol. Genet. Genomics
Abstract
Conserved synteny--the sharing of at least one orthologous gene by a pair of chromosomes from two species--can, in the strictest sense, be viewed as sequence conservation between chromosomes of two related species, irrespective of whether coding or non-coding sequence is examined. The recent sequencing of multiple vertebrate genomes indicates that certain chromosomal segments of considerable size are conserved in gene order as well as underlying non-coding sequence across all vertebrates. Some of these segments lost genes or non-coding sequence and/or underwent breakage only in teleost genomes, presumably because evolutionary pressure acting on these regions to remain intact were relaxed after an additional round of whole genome duplication. Random reporter insertions into zebrafish chromosomes combined with computational genome-wide analysis indicate that large chromosomal areas of multiple genes contain long-range regulatory elements, which act on their target genes from several gene distances away. In addition, computational breakpoint analyses suggest that recurrent evolutionary breaks are found in "fragile regions" or "hotspots", outside of the conserved blocks of synteny. These findings cannot be accommodated by the random breakage model and suggest that this view of genome and chromosomal evolution requires substantial reassessment.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping