The collapse of gene complement following whole genome duplication

BMC Genomics

Research Article

Qian Zhu¹  David Sankoff²  Chunfang Zheng³ 

[1] Department of Computer Science, Princeton University, 08544, Princeton, NJ, USA;Department of Mathematics and Statistics, University of Ottawa, K1N 6N5, Ottawa, Canada;Département d'informatique et de recherche opérationnelle, Université de Montréal, H3C 3J7, Montréal, Québec, Canada;

关键词: Geometric Distribution;    Whole Genome Doubling;    Analytical Unit;    Paralog Pair;    Whole Genome Doubling Event;   

DOI  :  10.1186/1471-2164-11-313

 received in 2009-08-19, accepted in 2010-05-19,  发布年份 2010

来源: Springer

【 摘 要 】

BackgroundGenome amplification through duplication or proliferation of transposable elements has its counterpart in genome reduction, by elimination of DNA or by gene inactivation. Whether loss is primarily due to excision of random length DNA fragments or the inactivation of one gene at a time is controversial. Reduction after whole genome duplication (WGD) represents an inexorable collapse in gene complement.ResultsWe compare fifteen genomes descending from six eukaryotic WGD events 20-450 Mya. We characterize the collapse over time through the distribution of runs of reduced paralog pairs in duplicated segments. Descendant genomes of the same WGD event behave as replicates. Choice of paralog pairs to be reduced is random except for some resistant regions of contiguous pairs. For those paralog pairs that are reduced, conserved copies tend to concentrate on one chromosome.ConclusionsBoth the contiguous regions of reduction-resistant pairs and the concentration of runs of single copy genes on a single chromosome are evidence of transcriptional co-regulation, dosage sensitivity or other functional interaction constraining the reduction process. These constraints and their evolution over time show a consistent pattern across evolutionary domains and a highly reproducible pattern, as replicates, for the several descendants of a single WGD.

【 授权许可】

CC BY   
© Sankoff et al; licensee BioMed Central Ltd. 2010