Evidence map›Paper›PMID 18711218›Full record

ReviewGenetics2008

Tilting at quixotic trait loci (QTL): an evolutionary perspective on genetic causation.

Kenneth M Weiss

Abstract readReview
In one paragraph

Review in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
–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

38 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Evolutionary psychiatry: foundations, progress and challenges.World psychiatry : official journal of the World Psychiatric Association (WPA) · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. The many faces of pleiotropy.Trends in genetics : TIG · 2013
    Article
  17. Article
  18. Article
  19. Article
  20. Evolution of a membrane protein regulon in Saccharomyces.Molecular biology and evolution · 2012
    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

1 author.

Kenneth M WeissDepartment of Anthropology and Integrated Biosciences Genetics Program, Pennsylvania State University, University Park, Pennsylvania 16802, USA. kenweiss@psu.edu

Funding

ANALYZE: Software for Joint Linkage and LD AnalysisR01MH063749 · NIMH · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TERWILLIGER, JOSEPH D · 2001 to 2005
$1.7M
NIMH NIH HHS MH063749NIMH NIH HHS R01 MH063749
6 · The paper itself

Abstract

Recent years have seen great advances in generating and analyzing data to identify the genetic architecture of biological traits. Human disease has understandably received intense research focus, and the genes responsible for most Mendelian diseases have successfully been identified. However, the same advances have shown a consistent if less satisfying pattern, in which complex traits are affected by variation in large numbers of genes, most of which have individually minor or statistically elusive effects, leaving the bulk of genetic etiology unaccounted for. This pattern applies to diverse and unrelated traits, not just disease, in basically all species, and is consistent with evolutionary expectations, raising challenging questions about the best way to approach and understand biological complexity.

Indexed as

Evolution, MolecularQuantitative Trait LociAnimalsChromosome MappingGenetics, PopulationGenetic VariationHumans

Identifiers

PMID18711218
PMCPMC2516055

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.