Evidence map›Paper›PMID 28295031›Full record

ArticleHeredity2017

X-linkage is not a general inhibitor of tissue-specific gene expression in Drosophila melanogaster.

E Argyridou, A K Huylmans, A Königer, J Parsch

Open access · bronzeAbstract read
In one paragraph

Article in Heredity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 39% of its field
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

4 citing papers in PubMed, 9 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

E ArgyridouDepartment of Biology II, Faculty of Biology, Ludwig-Maximilians-Universität München (LMU), Planegg-Martinsried, Germany.
A K HuylmansDepartment of Biology II, Faculty of Biology, Ludwig-Maximilians-Universität München (LMU), Planegg-Martinsried, Germany.
A KönigerDepartment of Biology II, Faculty of Biology, Ludwig-Maximilians-Universität München (LMU), Planegg-Martinsried, Germany.
J ParschDepartment of Biology II, Faculty of Biology, Ludwig-Maximilians-Universität München (LMU), Planegg-Martinsried, Germany.
Ludwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a consequence of its difference in copy number between males and females, the X chromosome is subject to unique evolutionary forces and gene regulatory mechanisms. Previous studies of Drosophila melanogaster have shown that the expression of X-linked, testis-specific reporter genes is suppressed in the male germline. However, it is not known whether this phenomenon is restricted to testis-expressed genes or if it is a more general property of genes with tissue-specific expression, which are also underrepresented on the X chromosome. To test this, we compared the expression of three tissue-specific reporter genes (ovary, accessory gland and Malpighian tubule) inserted at various autosomal and X-chromosomal locations. In contrast to testis-specific reporter genes, we found no reduction of X-linked expression in any of the other tissues. In accessory gland and Malpighian tubule, we detected higher expression of the X-linked reporter genes, which suggests that they are at least partially dosage compensated. We found no difference in the tissue-specificity of X-linked and autosomal reporter genes. These findings indicate that, in general, the X chromosome is not a detrimental environment for tissue-specific gene expression and that the suppression of X-linked expression is limited to the male germline.

Indexed as

Genes, InsectGenes, X-LinkedAnimalsDosage Compensation, GeneticDrosophila melanogasterFemaleMaleMalpighian TubulesOrgan SpecificityOvaryX Chromosome

Identifiers

PMID28295031
PMCPMC5520135
OpenAlexW2595113067

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.