Dataset Information

The accumulation of gene regulation through time.

ABSTRACT: Gene expression is governed by an intricate combination of transcription factors (TFs), microRNAs (miRNAs), splicing factors, and other regulators. Genes cannot support infinitely complex regulation due to sequence constraints and the increased likelihood of harmful errors. However, the upper limit of regulatory complexity in the genome is not known. Here, we provide evidence that human genes are currently not operating at their maximum capacity in terms of gene regulation. We analyze genes spanning the full spectrum of eukaryote evolution, from primate-specific genes to genes present in the eukaryote ancestor, and show that older genes tend to be bound by more TFs, have more conserved upstream sequences, generate more alternative isoforms, house more miRNA targets, and are more likely to be affected by nonsense-mediated decay and RNA editing. These results cannot be explained by overrepresentation of certain functional categories among younger or older genes. Furthermore, the increase in complexity is continuous over evolutionary time, without signs of saturation, leading to the conclusion that most genes, at least in the human genome, have the capacity to evolve even more complex gene regulation in the future.

SUBMITTER: Warnefors M

PROVIDER: S-EPMC3157833 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

The accumulation of gene regulation through time.

Warnefors Maria M Eyre-Walker Adam A

Genome biology and evolution 20110311

Gene expression is governed by an intricate combination of transcription factors (TFs), microRNAs (miRNAs), splicing factors, and other regulators. Genes cannot support infinitely complex regulation due to sequence constraints and the increased likelihood of harmful errors. However, the upper limit of regulatory complexity in the genome is not known. Here, we provide evidence that human genes are currently not operating at their maximum capacity in terms of gene regulation. We analyze genes span ...[more]

PMID: 21398425

Similar Datasets

Project description:BACKGROUND: The molecular mechanisms that modify genome structures to give birth and death to alleles are still not well understood. To investigate the causative chromosomal rearrangements, we took advantage of the allelic diversity of the duplicated p1 and p2 genes in maize. Both genes encode a transcription factor involved in maysin synthesis, which confers resistance to corn earworm. However, p1 also controls accumulation of reddish pigments in floral tissues and has therefore acquired a new function after gene duplication. p1 alleles vary in their tissue-specific expression, which is indicated in their allele designation: the first suffix refers to red or white pericarp pigmentation and the second to red or white glume pigmentation. RESULTS: Comparing chromosomal regions comprising p1-ww[4Co63], P1-rw1077 and P1-rr4B2 alleles with that of the reference genome, P1-wr[B73], enabled us to reconstruct additive events of transposition, chromosome breaks and repairs, and recombination that resulted in phenotypic variation and chimeric regulatory signals. The p1-ww[4Co63] null allele is probably derived from P1-wr[B73] by unequal crossover between large flanking sequences. A transposon insertion in a P1-wr-like allele and NHEJ (non-homologous end-joining) could have resulted in the formation of the P1-rw1077 allele. A second NHEJ event, followed by unequal crossover, probably led to the duplication of an enhancer region, creating the P1-rr4B2 allele. Moreover, a rather dynamic picture emerged in the use of polyadenylation signals by different p1 alleles. Interestingly, p1 alleles can be placed on both sides of a large retrotransposon cluster through recombination, while functional p2 alleles have only been found proximal to the cluster. CONCLUSIONS: Allelic diversity of the p locus exemplifies how gene duplications promote phenotypic variability through composite regulatory signals. Transposition events increase the level of genomic complexity based not only on insertions but also on excisions that cause DNA double-strand breaks and trigger illegitimate recombination.

Dataset Information

The accumulation of gene regulation through time.

Publications

The accumulation of gene regulation through time.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets