Evidence map›Paper›PMID 33644714›Full record

ArticleiScience2021

Telomere length dynamics in response to DNA damage in malaria parasites.

Jake Reed, Laura A Kirkman, Björn F Kafsack, Christopher E Mason, Kirk W Deitsch

Open access · goldAbstract read
In one paragraph

Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Frontiers in cellular and infection microbiology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. 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

5 authors at 1 institution in 1 country.

Jake ReedDepartment of Microbiology and Immunology, Weill Cornell Medical College, New York, NY, USA.
Laura A KirkmanDepartment of Microbiology and Immunology, Weill Cornell Medical College, New York, NY, USA.
Björn F KafsackDepartment of Microbiology and Immunology, Weill Cornell Medical College, New York, NY, USA.
Christopher E MasonDepartment of Physiology and Biophysics, Weill Cornell Medical College, New York, NY, USA.
Kirk W DeitschDepartment of Microbiology and Immunology, Weill Cornell Medical College, New York, NY, USA.
Cornell University · US

Funding

Var gene regulation and antigenic variation in malariaR01AI052390 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI DEITSCH, KIRK W · 2002 to 2019
$6.6M
Mechanisms of environmental sensing and responses by malaria parasitesR01AI138499 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI DEITSCH, KIRK W · 2018 to 2022
$3.7M
Role of Translesional Polymerases in Genome Diversification of the Malaria ParasiteR01AI146153 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI KIRKMAN, LAURA · 2019 to 2023
$3.1M
DNA repair and recombination within the var gene family of P. falciparumR01AI099327 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI DEITSCH, KIRK W · 2012 to 2016
$2.2M
NIAID NIH HHS R01 AI052390NIAID NIH HHS R01 AI099327NIAID NIH HHS R01 AI138499NIAID NIH HHS R01 AI146153
6 · The paper itself

Abstract

Malaria remains a major cause of morbidity and mortality in the developing world. Recent work has implicated chromosome end stability and the repair of DNA breaks through telomere healing as potent drivers of variant antigen diversification, thus associating basic mechanisms for maintaining genome integrity with aspects of host-parasite interactions. Here we applied long-read sequencing technology to precisely examine the dynamics of telomere addition and chromosome end stabilization in response to double-strand breaks within subtelomeric regions. We observed that the process of telomere healing induces the initial synthesis of telomere repeats well in excess of the minimal number required for end stability. However, once stabilized, these newly created telomeres appear to function normally, eventually returning to a length nearing that of intact chromosome ends. These results parallel recent observations in humans, suggesting an evolutionarily conserved mechanism for chromosome end repair.

Indexed as

astrobiologychromosome organizationomicsparasitology

Identifiers

PMID33644714
PMCPMC7887396
OpenAlexW3122139960

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.