Evidence map›Paper›PMID 10373558›Full record

ArticleMolecular and cellular biology1999

Atm inactivation results in aberrant telomere clustering during meiotic prophase.

T K Pandita, C H Westphal, M Anger, S G Sawant, C R Geard, R K Pandita, H Scherthan

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 89 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 4 institutions in 2 countries.

T K PanditaColumbia University, New York, New York 10032, USA. tkp1@columbia.edu
C H Westphal
M Anger
S G Sawant
C R Geard
R K Pandita
H Scherthan
Columbia University · USUniversity of Kaiserslautern · DEAlbert Einstein College of Medicine · USHarvard University · US

Funding

CHROMATIN-TELOMERE STRUCTURE AND AT GENOMIC SENSITIVITYR01NS034746 · NINDS · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 1996 to 2005
$1.2M
NINDS NIH HHS NS34746NINDS NIH HHS R01 NS034746
6 · The paper itself

Abstract

A-T (ataxia telangiectasia) individuals frequently display gonadal atrophy, and Atm-/- mice show spermatogenic failure due to arrest at prophase of meiosis I. Chromosomal movements take place during meiotic prophase, with telomeres congregating on the nuclear envelope to transiently form a cluster during the leptotene/zygotene transition (bouquet arrangement). Since the ATM protein has been implicated in telomere metabolism of somatic cells, we have set out to investigate the effects of Atm inactivation on meiotic telomere behavior. Fluorescent in situ hybridization and synaptonemal complex (SC) immunostaining of structurally preserved spermatocytes I revealed that telomere clustering occurs aberrantly in Atm-/- mice. Numerous spermatocytes of Atm-/- mice displayed locally accumulated telomeres with stretches of SC near the clustered chromosome ends. This contrasted with spermatogenesis of normal mice, where only a few leptotene/zygotene spermatocytes I with clustered telomeres were detected. Pachytene nuclei, which were much more abundant in normal mice, displayed telomeres scattered over the nuclear periphery. It appears that the timing and occurrence of chromosome polarization is altered in Atm-/- mice. When we examined telomere-nuclear matrix interactions in spermatocytes I, a significant difference was observed in the ratio of soluble versus matrix-associated telomeric DNA sequences between meiocytes of Atm-/- and control mice. We propose that the severe disruption of spermatogenesis during early prophase I in the absence of functional Atm may be partly due to altered interactions of telomeres with the nuclear matrix and distorted meiotic telomere clustering.

Indexed as

Ataxia TelangiectasiaChromosome AberrationsProtein Serine-Threonine KinasesTelomereAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA-Binding ProteinsGene ExpressionMaleMeiosisMiceMice, KnockoutNuclear MatrixProphaseProteinsAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsProteinsProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID10373558
PMCPMC84352
OpenAlexW2130025112

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.