Evidence map›Paper›PMID 32842932›Full record

ArticleProceedings. Biological sciences2020

Genome size evolution: towards new model systems for old questions.

Julie Blommaert

Abstract read
In one paragraph

Article in Proceedings. Biological sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing 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

68 citing papers in PubMed.

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  9. Genome size estimation and evolution trends in Acari.Experimental & applied acarology · 2025
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8 more citing papers are in PubMed but not listed here.

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.

Julie BlommaertDepartment of Organismal Biology, Uppsala University, Uppsala, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome size (GS) variation is a fundamental biological characteristic; however, its evolutionary causes and consequences are the topic of ongoing debate. Whether GS is a neutral trait or one subject to selective pressures, and how strong these selective pressures are, may remain open questions. Fundamentally, the genomic sequences responsible for this variation directly impact the potential evolutionary outcomes and, equally, are the targets of different evolutionary pressures. For example, duplications and deletions of genic regions (large or small) can have immediate and drastic phenotypic effects, while an expansion or contraction of non-coding DNA is less likely to cause catastrophic phenotypic effects. However, in the long term, the accumulation or deletion of ncDNA is likely to have larger effects. Modern sequencing technologies are allowing for the dissection of these proximate causes, but a combination of these new technologies with more traditional evolutionary experiments and approaches could revolutionize this debate and potentially resolve many of these arguments. Here, I discuss an ambitious way forward for GS research, putting it in context of historical debates, theories and sometimes contradictory evidence, and highlighting the promise of combining new sequencing technologies and analytical developments with more traditional experimental evolution approaches.

Indexed as

Evolution, MolecularGenome SizeAnimalsGenomicsexperimental evolutiongenomicslong-read sequencingnext-generation sequencing

Identifiers

PMID32842932
PMCPMC7482279

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.