Evidence map›Paper›PMID 10931920›Full record

ArticleNucleic acids research2000

CHL1 is a nuclear protein with an essential ATP binding site that exhibits a size-dependent effect on chromosome segregation.

S L Holloway

Open access · bronzeAbstract read
In one paragraph

Article in Nucleic acids research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.1field-weighted citation impact, top 51% of its field
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

22 citing papers in PubMed, 35 citations in OpenAlex.

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  7. Role of the DDX11 DNA Helicase in Warsaw Breakage Syndrome Etiology.International journal of molecular sciences · 2021
    Review
  8. Spotlight on Warsaw Breakage Syndrome.The application of clinical genetics · 2019
    Review
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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 at 1 institution in 1 country.

S L HollowayHoward Hughes Medical Institute, Department of Genetics, University of Pennsylvania, 415 Curie Boulevard, Philadelphia, PA 19104, USA. hollowas@mail.med.upenn.edu
University of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Saccharomyces cerevisiae chl1 mutants have a significant increase in the rate of chromosome missegregation. CHL1 encodes a 99 kDa predicted protein with an ATP binding site consensus, a putative helix-turn-helix DNA binding motif, and homology to helicases. Using site-directed mutagenesis, I show that mutations that are predicted to abolish ATP binding in CHL1 inactivate its function in chromosome segregation. Furthermore, overexpression of these mutations interferes with chromosome transmission of a 125 kb chromosome fragment in a wild-type strain. Polyclonal antibodies against CHL1 show that CHL1 is predominantly in the nuclear fraction of S. CEREVISIAE: CHL1 function is more critical for the segregation of small chromosomes. In chl1Delta1/chl1Delta1 mutants, artificial circular or linear chromosomes <150 kb in size exhibit near random segregation (0.12 per cell division), whereas all chromosomes tested >225 kb were lost at rates (5 x 10(-)(3) per cell division) comparable to that observed for endogenous chromosome III. These results reveal an important role for ATPases/DNA helicases in chromosome segregation. Such enzymes may alter DNA topology to allow loading of proteins involved in maintaining sister chromatid cohesion.

Indexed as

Saccharomyces cerevisiae ProteinsAdenosine TriphosphatasesAdenosine TriphosphateAmino Acid SequenceAmino Acid SubstitutionBinding SitesChromosomal Proteins, Non-HistoneChromosomes, FungalConsensus SequenceDNAFungal ProteinsHumansMutagenesis, Site-DirectedPoint MutationRecombinant ProteinsSaccharomyces cerevisiaeAdenosine TriphosphatasesAdenosine TriphosphateCHL1 protein, S cerevisiaeChromosomal Proteins, Non-HistoneDNAFungal ProteinsRecombinant ProteinsSaccharomyces cerevisiae Proteins

Identifiers

PMID10931920
PMCPMC108448
OpenAlexW2102699094

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.