Evidence map›Paper›PMID 18780755›Full record

ArticleGenetics2008

Positive selection at the binding sites of the male-specific lethal complex involved in dosage compensation in Drosophila.

Doris Bachtrog

Abstract read
In one paragraph

Article in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. GFZF, a GlutathioneMolecular and cellular biology · 2018
    Article
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  12. Article
  13. Article
  14. Review
  15. Article
  16. Progress and prospects toward our understanding of the evolution of dosage compensation.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2009
    Review
  17. Review
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

1 author.

Doris BachtrogDepartment of Integrative Biology, University of California, Berkeley, California 94720, USA. dbachtrog@berkeley.edu

Funding

The evolution of dosage compensation in DrosophilaR01GM076007 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BACHTROG, DORIS · 2006 to 2020
$3.6M
NIGMS NIH HHS GM-076007NIGMS NIH HHS R01 GM076007
6 · The paper itself

Abstract

In many taxa, males and females differ with respect to their sex chromosomes, and dosage compensation mechanisms have evolved to equalize X-linked gene transcription. In Drosophila, the male-specific lethal (MSL) complex binds to hundreds of sites along the male X chromosome and mediates twofold hypertranscription of the single male X. Two recent studies found evidence for lineage-specific adaptive evolution in all five core protein-coding genes of the MSL complex in Drosophila melanogaster. In particular, dramatic positive selection was detected in domains shown to be responsible for their specific targeting to the X chromosome. Here I use population genetics to show that three previously characterized MSL-binding DNA segments on the X themselves underwent adaptive evolution in D. melanogaster, but not in its close relatives D. simulans and D. yakuba. MSL components have been shown to not correctly target the D. melanogaster X chromosome in hybrids between D. melanogaster and D. simulans. My finding supports the idea of selection-driven coevolution among DNA-protein interactions of the dosage compensation machinery and suggests that misregulated dosage compensation could contribute to male hybrid inviability in Drosophila.

Indexed as

Dosage Compensation, GeneticAnimalsBinding SitesDNA-Binding ProteinsDrosophilaEvolution, MolecularGenetics, PopulationMaleNuclear ProteinsSelection, GeneticX ChromosomeDNA-Binding ProteinsNuclear Proteins

Identifiers

PMID18780755
PMCPMC2567361

What OpenQuestion holds

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Registered trials

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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.