Evidence map›Paper›PMID 12196390›Full record

ArticleGenetics2002

A heritable structural alteration of the yeast mitochondrion.

Daniel Lockshon

Abstract read
In one paragraph

Article in Genetics, 2002. 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
–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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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.

Daniel LockshonDepartment of Genetics, University of Washington, Seattle, Washington 98195, USA. lockshon@u.washington.edu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prions have revived interest in hereditary change that is due to change in cellular structure. How pervasive is structural inheritance and what are its mechanisms? Described here is the initial characterization of [Leu(P)], a heritable structural change of the mitochondrion of Saccharomyces cerevisiae that often but not always accompanies the loss of all or part of the mitochondrial genome. Three phenotypes are reported in [Leu(P)] vs. [Leu(+)] strains: twofold slower growth, threefold slower growth in the absence of leucine, and a marked delocalization of nuclear-encoded protein destined for the mitochondrion. Introduction of mitochondria from a [Leu(+)] strain by cytoduction can convert a [Leu(P)] strain to [Leu(+)] and vice versa. Evidence against the Mendelian inheritance of the trait is presented. The incomplete dominance of [Leu(P)] and [Leu(+)] and the failure of HSP104 deletion to have any effect suggest that the trait is not specified by a prion but instead represents a new class of heritable structural change.

Indexed as

Heat-Shock ProteinsLeucineMitochondriaPrionsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsHeat-Shock ProteinsHsP104 protein, S cerevisiaeLeucinePrionsSaccharomyces cerevisiae Proteins

Identifiers

PMID12196390
PMCPMC1462224

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.