Evidence map›Paper›PMID 7860059›Full record

ReviewHuman genetics1995

The genetic contribution to the phenotype.

U Wolf

Abstract readReview
PubMed Publisher
In one paragraph

Review in Human genetics, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
  2. Review
  3. Male-specific repeats in wild Bovidae.Journal of applied genetics · 2012
    Article
  4. Article
  5. Review
  6. The nature and significance of behavioural genetic information.Theoretical medicine and bioethics · 2004
    Review
  7. Human gene mutation in pathology and evolution.Journal of inherited metabolic disease · 2002
    Review
  8. Review
  9. Schizophrenia epigenesis?Theoretical medicine and bioethics · 2000
    Review
  10. Review
  11. Review
  12. Gene environment interaction.Journal of epidemiology and community health · 1996
    Review
  13. Article
  14. Genetic complexity in single gene diseases.BMJ (Clinical research ed.) · 1996
    Article
  15. 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.

U WolfInstitut für Humangenetik und Anthropologie, Universität Freiburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The phenotype is the result of ontogenetic development. This holds true also at the molecular level, because molecular biological processes take place within the organism. In ontogenesis, genetic and nongenetic factors interact in producing successive states, each of which is the prerequisite, and determines the conditions, for the next one to follow. In this interplay, genes are a necessary, but not sufficient, component. The structures already present, gradients, threshold values, positional relationships, and conditions of the internal milieu, are equally essential. Thus, even monofactorial traits can be considered to be of multifactorial causation, and the varying borderline conditions that arise during development add to the complexity. From this standpoint, it is not to be expected that a mutation has a consistent phenotypic outcome, and the genotype-phenotype relationship may be irregular. In the present review, genotypic heterogeneity versus phenotypic heterogeneity is discussed with the help of some selected examples of hereditary diseases. Conditions and mechanisms contributing to this heterogeneity are addressed. It is concluded that the genotype-phenotype relationship is neither unidimensional, programmatical nor hierarchical in a strict sense. Nevertheless, in particular cases, ontogenetic modification appears to be of minor significance, so that the phenotype of a mutation can be predicted with considerable accuracy. This is no surprise if, depending on the nature of the mutation and the physiological function of the gene affected, the genotype-phenotype relationship is direct. However, this relationship may also be consistent in more complex conditions. It is assumed that the total of the non-genetic influences (epigenetic, environmental) are usually so similar or are compensated by the organism to such an extent that the respective mutation acts as the major variable during ontogenetic development.

Indexed as

PhenotypeGenotypeHumans

Identifiers

PMID7860059

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.