Evidence map›Paper›PMID 18846223›Full record

ArticlePloS one2008

A non-canonical function of zebrafish telomerase reverse transcriptase is required for developmental hematopoiesis.

Shintaro Imamura, Junzo Uchiyama, Eriko Koshimizu, Jun-Ichi Hanai, Christina Raftopoulou, Ryan D Murphey, Peter E Bayliss, Yoichi Imai, Caroline Erter Burns, Kenkichi Masutomi and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

37 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Observational
  5. Inflammation in Development and Aging: Insights from the Zebrafish Model.International journal of molecular sciences · 2024
    Review
  6. iScience · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Non-canonical Roles of Telomerase: Unraveling the Imbroglio.Frontiers in cell and developmental biology · 2019
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. The age of heterozygousWellcome open research · 2017
    Article
  17. Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 8 institutions in 3 countries.

Shintaro ImamuraSchepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA.
Junzo Uchiyama
Eriko Koshimizu
Jun-Ichi Hanai
Christina Raftopoulou
Ryan D Murphey
Peter E Bayliss
Yoichi Imai
Caroline Erter Burns
Kenkichi Masutomi
Sarantis Gagos
Leonard I Zon
Thomas M Roberts
Shuji Kishi
Harvard University · USBiomedical Research Foundation of the Academy of Athens · GRHoward Hughes Medical Institute · USBeth Israel Deaconess Medical Center · USDana-Farber Cancer Institute · USMassachusetts Eye and Ear Infirmary · USNational Cancer Centre Japan · JPSmith-Kettlewell Eye Research Institute · US

Funding

Definitive Hematopoiesis in ZebrafishK01DK067179 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI BURNS, CAROLINE E · 2005 to 2009
$632k
NIDDK NIH HHS K01 DK067179
6 · The paper itself

Abstract

Although it is clear that telomerase expression is crucial for the maintenance of telomere homeostasis, there is increasing evidence that the TERT protein can have physiological roles that are independent of this central function. To further examine the role of telomerase during vertebrate development, the zebrafish telomerase reverse transcriptase (zTERT) was functionally characterized. Upon zTERT knockdown, zebrafish embryos show reduced telomerase activity and are viable, but develop pancytopenia resulting from aberrant hematopoiesis. The blood cell counts in TERT-depleted zebrafish embryos are markedly decreased and hematopoietic cell differentiation is impaired, whereas other somatic lineages remain morphologically unaffected. Although both primitive and definitive hematopoiesis is disrupted by zTERT knockdown, the telomere lengths are not significantly altered throughout early development. Induced p53 deficiency, as well as overexpression of the anti-apoptotic proteins Bcl-2 and E1B-19K, significantly relieves the decreased blood cells numbers caused by zTERT knockdown, but not the impaired blood cell differentiation. Surprisingly, only the reverse transcriptase motifs of zTERT are crucial, but the telomerase RNA-binding domain of zTERT is not required, for rescuing complete hematopoiesis. This is therefore the first demonstration of a non-canonical catalytic activity of TERT, which is different from "authentic" telomerase activity, is required for during vertebrate hematopoiesis. On the other hand, zTERT deficiency induced a defect in hematopoiesis through a potent and specific effect on the gene expression of key regulators in the absence of telomere dysfunction. These results suggest that TERT non-canonically functions in hematopoietic cell differentiation and survival in vertebrates, independently of its role in telomere homeostasis. The data also provide insights into a non-canonical pathway by which TERT functions to modulate specification of hematopoietic stem/progenitor cells during vertebrate development. (276 words).

Indexed as

AnimalsApoptosisCell DifferentiationCell SurvivalEmbryo, NonmammalianHematopoiesisHematopoietic Stem CellsHomeostasisHumansIn Situ HybridizationOligonucleotides, AntisenseRecombinant Fusion ProteinsTelomeraseTelomereTumor Suppressor Protein p53ZebrafishOligonucleotides, AntisenseRecombinant Fusion ProteinsTelomeraseTumor Suppressor Protein p53

Identifiers

PMID18846223
PMCPMC2561060
OpenAlexW2063509106

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.