Abstract
Fish-mammal genomic alignments were used to compare over 800 conserved non-coding elements that associate with genes that have undergone fish-specific duplication and retention, revealing a pattern of element retention and loss between paralogs indicative of subfunctionalization.
Highlights
A major mechanism for the preservation of gene duplicates in the genome is thought to be mediated via loss or modification of cis-regulatory subfunctions between paralogs following duplication
We selected seven genomic regions in human that fitted this criterion, each containing clusters of coding elements (CNEs) in the vicinity of a single gene implicated in developmental regulation: BCL11A, EBF1, FIGN, PAX2, SOX1 (HMG box transcription factor Sox1), UNC4.1 and ZNF503
We identified potential gene candidates that contain both CNEs in their vicinity and are likely to derive from fish-specific duplication events using data from the initial whole genome comparison of the Fugu and human genomes
Summary
A major mechanism for the preservation of gene duplicates in the genome is thought to be mediated via loss or modification of cis-regulatory subfunctions between paralogs following duplication (a process known as regulatory subfunctionalization). Several studies suggest that the proportion of duplicated genes retained in vertebrate genomes is much higher than is predicted by this model [4,5,6] This has led to the suggestion of an alternative model whereby complementary degenerative mutations in independent subfunctions of each gene copy permits their preservation in the genome, as both copies of the gene are required to recapitulate the full range of functions present in the single ancestral gene. This was formalized in the Duplication-Degeneration-Complementation (DDC) model [7] in a process referred to as subfunctionalization
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