Evidence map›Paper›PMID 10581268›Full record

ArticleGenetics1999

Frequent meiotic recombination between the ends of truncated chromosome fragments of Saccharomyces cerevisiae.

T Arbel, R Shemesh, G Simchen

Abstract read
In one paragraph

Article in Genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

3 authors.

T ArbelDepartment of Genetics, The Hebrew University of Jerusalem, Jerusalem 91904, Israel.
R Shemesh
G Simchen

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A single truncated chromosome fragment (TCF) in diploid cells undergoes frequent ectopic recombination during meiosis between markers located near the ends of the fragment. Tetrads produced by diploids with a single TCF show frequent loss of one of the two markers. This marker loss could result either from recombination of the TCF with one of the two copies of the chromosome from which it was derived or from ectopic recombination between the ends of the TCF. The former would result in shortening of a normal chromosome and lethality in one of the four spores. The high frequency of marker loss in tetrads with four viable spores supports recombination between the TCF ends as the main source of marker loss. Most of the spore colonies that display TCF marker loss contained a TCF with the same marker on both ends. Deletion of most of the pBR322 sequences distal to the marker at one of the subtelomeric regions of the TCF did not reduce the overall frequency of recombination between the ends, but affected the loss of one marker significantly more than the other. We suggest that the mechanism by which the duplication of one end marker and loss of the other occurs is based on association and recombination between the ends of the TCF.

Indexed as

Chromosomes, FungalRecombination, GeneticGenetic MarkersHaploidyMeiosisPlasmidsSaccharomyces cerevisiaeGenetic Markers

Identifiers

PMID10581268
PMCPMC1460867

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.