Evidence map›Paper›PMID 19635763›Full record

ReviewThe Journal of heredity

A surrogate approach to study the evolution of noncoding DNA elements that organize eukaryotic genomes.

Danielle Vermaak, Joshua J Bayes, Harmit S Malik

Abstract readReview
In one paragraph

Review in The Journal of heredity. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Danielle VermaakDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
Joshua J Bayes
Harmit S Malik

Funding

TRAINING IN MOLECULAR AND CELLULAR BIOLOGYT32GM007270 · NIGMS · UNIVERSITY OF WASHINGTON · PI RAIBLE, DAVID W · 1985 to 2020
$21.0M
Genetic Conflict Shapes Centromeres and HeterochromatinR01GM074108 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI MALIK, HARMIT S. · 2005 to 2022
$6.1M
NIGMS NIH HHS R01 GM074108NIGMS NIH HHS R01-GM074108NIGMS NIH HHS T32 GM07270
6 · The paper itself

Abstract

Comparative genomics provides a facile way to address issues of evolutionary constraint acting on different elements of the genome. However, several important DNA elements have not reaped the benefits of this new approach. Some have proved intractable to current day sequencing technology. These include centromeric and heterochromatic DNA, which are essential for chromosome segregation as well as gene regulation, but the highly repetitive nature of the DNA sequences in these regions make them difficult to assemble into longer contigs. Other sequences, like dosage compensation X chromosomal sites, origins of DNA replication, or heterochromatic sequences that encode piwi-associated RNAs, have proved difficult to study because they do not have recognizable DNA features that allow them to be described functionally or computationally. We have employed an alternate approach to the direct study of these DNA elements. By using proteins that specifically bind these noncoding DNAs as surrogates, we can indirectly assay the evolutionary constraints acting on these important DNA elements. We review the impact that such "surrogate strategies" have had on our understanding of the evolutionary constraints shaping centromeres, origins of DNA replication, and dosage compensation X chromosomal sites. These have begun to reveal that in contrast to the view that such structural DNA elements are either highly constrained (under purifying selection) or free to drift (under neutral evolution), some of them may instead be shaped by adaptive evolution and genetic conflicts (these are not mutually exclusive). These insights also help to explain why the same elements (e.g., centromeres and replication origins), which are so complex in some eukaryotic genomes, can be simple and well defined in other where similar conflicts do not exist.

Indexed as

Evolution, MolecularGenomeAnimalsCell Cycle ProteinsCentromereComparative Genomic HybridizationDNADNA-Binding ProteinsDNA ReplicationDosage Compensation, GeneticDrosophila ProteinsEpigenesis, GeneticHistonesMeiosisModels, GeneticSelection, GeneticCdc6 protein, DrosophilaCell Cycle ProteinsDNADNA-Binding ProteinsDrosophila ProteinsHistones

Identifiers

PMID19635763
PMCPMC2877547

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.