Evidence map›Paper›PMID 17726166›Full record

ArticleGenome research2007

A model of segmental duplication formation in Drosophila melanogaster.

Anna-Sophie Fiston-Lavier, Dominique Anxolabehere, Hadi Quesneville

Abstract read
In one paragraph

Article in Genome research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing 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

47 citing papers in PubMed.

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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.

Anna-Sophie Fiston-LavierLaboratoire Bioinformatique et Génomique, Institut Jacques Monod, 75005 Paris, France.
Dominique Anxolabehere
Hadi Quesneville

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Segmental duplications (SDs) are low-copy repeats of DNA segments that have long been recognized to be involved in genome organization and evolution. But, to date, the mechanism of their formation remains obscure. We propose a model for SD formation that we name "duplication-dependent strand annealing" (DDSA). This model is a variant of the synthesis-dependent strand annealing (SDSA) model--a double-strand break (DSB) homologous repair model. DSB repair in Drosophila melanogaster genome usually occurs primarily through homologous repair, more preferentially through the SDSA model. The DDSA model predicts that after a DSB, the search for an ectopic homologous region--here a repeat--initiates the repair. As expected by the model, the analysis of SDs detected by a computational analysis of the D. melanogaster genome indicates a high enrichment in transposable elements at SD ends. It shows moreover a preferential location of SDs in heterochromatic regions. The model has the advantage of also predicting specific traces left during synthesis. The observed traces support the DDSA model as one model of formation of SDs in D. melanogaster genome. The analysis of these DDSA signatures suggests moreover a sequestration of the dissociated strand in the repair complex.

Indexed as

Gene DuplicationModels, GeneticAnimalsBase SequenceDNADNA Breaks, Double-StrandedDNA RepairDrosophila melanogasterGenes, InsectGenome, InsectHeterochromatinMolecular Sequence DataRepetitive Sequences, Nucleic AcidSequence Homology, Nucleic AcidTandem Repeat SequencesDNAHeterochromatin

Identifiers

PMID17726166
PMCPMC1987339

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.