Evidence map›Paper›PMID 34718547›Full record

ArticleG3 (Bethesda, Md.)2021

Suppression of telomere capping defects of Saccharomyces cerevisiae yku70 and yku80 mutants by telomerase.

Cory L Holland, Brian A Sanderson, James K Titus, Monica F Weis, Angelica M Riojas, Eric Malczewskyj, Brian M Wasko, L Kevin Lewis

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in G3 (Bethesda, Md.), 2021. 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
0.1field-weighted citation impact, top 55% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Review
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

8 authors at 2 institutions in 1 country.

Cory L HollandDepartment of Chemistry and Biochemistry, Texas State University, San Marcos, TX 78666, USA.
Brian A SandersonDepartment of Chemistry and Biochemistry, Texas State University, San Marcos, TX 78666, USA.
James K TitusDepartment of Chemistry and Biochemistry, Texas State University, San Marcos, TX 78666, USA.
Monica F WeisDepartment of Chemistry and Biochemistry, Texas State University, San Marcos, TX 78666, USA.
Angelica M RiojasDepartment of Chemistry and Biochemistry, Texas State University, San Marcos, TX 78666, USA.
Eric MalczewskyjDepartment of Chemistry and Biochemistry, Texas State University, San Marcos, TX 78666, USA.
Brian M WaskoDepartment of Biology and Biotechnology, University of Houston-Clear Lake, Houston, TX, 77058, USA.ORCID 0000-0002-7090-086X
L Kevin LewisDepartment of Chemistry and Biochemistry, Texas State University, San Marcos, TX 78666, USA.
Texas State University · USUniversity of Houston - Clear Lake · US

Funding

South Texas Doctoral Bridge ProgramR25GM102783 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI OYAJOBI, BABATUNDE OLUKAYODE, WHITTEN, STEVEN T · 2013 to 2022
$3.1M
DNA repair pathways preserve cellular homeostasisR15GM139093 · NIGMS · TEXAS STATE UNIVERSITY · PI LEWIS, LYSLE KEVIN · 2020 to 2020
$440k
NIGMS NIH HHS R15 GM139093NIGMS NIH HHS R25 GM102783
6 · The paper itself

Abstract

The Ku complex performs multiple functions inside eukaryotic cells, including protection of chromosomal DNA ends from degradation and fusion events, recruitment of telomerase, and repair of double-strand breaks (DSBs). Inactivation of Ku complex genes YKU70 or YKU80 in cells of the yeast Saccharomyces cerevisiae gives rise to mutants that exhibit shortened telomeres and temperature-sensitive growth. In this study, we have investigated the mechanism by which overexpression of telomerase suppresses the temperature sensitivity of yku mutants. Viability of yku cells was restored by overexpression of the Est2 reverse transcriptase and TLC1 RNA template subunits of telomerase, but not the Est1 or Est3 proteins. Overexpression of other telomerase- and telomere-associated proteins (Cdc13, Stn1, Ten1, Rif1, Rif2, Sir3, and Sir4) did not suppress the growth defects of yku70 cells. Mechanistic features of suppression were assessed using several TLC1 RNA deletion derivatives and Est2 enzyme mutants. Supraphysiological levels of three catalytically inactive reverse transcriptase mutants (Est2-D530A, Est2-D670A, and Est2-D671A) suppressed the loss of viability as efficiently as the wild-type Est2 protein, without inducing cell senescence. Roles of proteins regulating telomere length were also determined. The results support a model in which chromosomes in yku mutants are stabilized via a replication-independent mechanism involving structural reinforcement of protective telomere cap structures.

Indexed as

Saccharomyces cerevisiae ProteinsTelomeraseDNA-Binding ProteinsRepressor ProteinsSaccharomyces cerevisiaeSilent Information Regulator Proteins, Saccharomyces cerevisiaeTelomereTelomere-Binding ProteinsCdc13 protein, S cerevisiaeDNA-Binding ProteinsEST1 protein, S cerevisiaeEST3 protein, S cerevisiaeRepressor ProteinsRIF1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSIR3 protein, S cerevisiaeTelomeraseTelomere-Binding ProteinsYKU70 protein, S cerevisiaeYKU80 protein, S cerevisiaecheckpointDNA repairend-joiningrecombinationreplicationsenescencetelomerase

Identifiers

PMID34718547
PMCPMC8664480
OpenAlexW3206906420

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.