Evidence map›Paper›PMID 16705169›Full record

ArticleMolecular and cellular biology2006

Cathepsin L stabilizes the histone modification landscape on the Y chromosome and pericentromeric heterochromatin.

Yaroslava A Bulynko, Lianne C Hsing, Robert W Mason, David J Tremethick, Sergei A Grigoryev

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In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  10. Review
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  14. Specialized roles for cysteine cathepsins in health and disease.The Journal of clinical investigation · 2010
    Review
  15. Review
  16. Article
  17. Stefin B interacts with histones and cathepsin L in the nucleus.The Journal of biological chemistry · 2010
    Article
  18. Article
  19. Article
  20. Chromatin condensation in terminally differentiating mouse erythroblasts does not involve special architectural proteins but depends on histone deacetylation.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2009
    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 4 institutions in 2 countries.

Yaroslava A BulynkoPenn State University College of Medicine, Department of Biochemistry and Molecular Biology, H171, Milton S. Hershey Medical Center, P.O. Box 850, 500 University Drive, Hershey, PA 17033, USA.
Lianne C Hsing
Robert W Mason
David J Tremethick
Sergei A Grigoryev
Penn State Milton S. Hershey Medical Center · USAlfred I. duPont Hospital for Children · USAustralian National University · AUHoward Hughes Medical Institute · US

Funding

TRAJECTORIES OF CHANGE IN BMI STATUS IN EARLY CHILDHOODP20RR020173 · NCRR · NEMOURS CHILDREN'S HOSPITAL, DELAWARE · PI MASON, ROBERT · 2004 to 2011
$14.9M
NCRR NIH HHS 5P20RR020173NCRR NIH HHS P20 RR020173
6 · The paper itself

Abstract

Posttranslational histone modifications and histone variants form a unique epigenetic landscape on mammalian chromosomes where the principal epigenetic heterochromatin markers, trimethylated histone H3(K9) and the histone H2A.Z, are inversely localized in relation to each other. Trimethylated H3(K9) marks pericentromeric constitutive heterochromatin and the male Y chromosome, while H2A.Z is dramatically reduced at these chromosomal locations. Inactivation of a lysosomal and nuclear protease, cathepsin L, causes a global redistribution of epigenetic markers. In cathepsin L knockout cells, the levels of trimethylated H3(K9) decrease dramatically, concomitant with its relocation away from heterochromatin, and H2A.Z becomes enriched at pericentromeric heterochromatin and the Y chromosome. This change is also associated with global relocation of heterochromatin protein HP1 and histone H3 methyltransferase Suv39h1 away from constitutive heterochromatin; however, it does not affect DNA methylation or chromosome segregation, phenotypes commonly associated with impaired histone H3(K9) methylation. Therefore, the key constitutive heterochromatin determinants can dynamically redistribute depending on physiological context but still maintain the essential function(s) of chromosomes. Thus, our data show that cathepsin L stabilizes epigenetic heterochromatin markers on pericentromeric heterochromatin and the Y chromosome through a novel mechanism that does not involve DNA methylation or affect heterochromatin structure and operates on both somatic and sex chromosomes.

Indexed as

ThermodynamicsAnimalsCathepsin LCathepsinsCell NucleusCentromereChromatinChromosome SegregationChromosomes, MammalianCysteine EndopeptidasesDNA MethylationEpigenesis, GeneticFibroblastsGene ExpressionGenetic MarkersHeterochromatinCathepsin LCathepsinsChromatinCTSL protein, humanCtsl protein, mouseCysteine EndopeptidasesGenetic MarkersHeterochromatinHistonesLysineMethyltransferasesRepressor ProteinsSuv39h1 protein, mouse

Identifiers

PMID16705169
PMCPMC1489105
OpenAlexW2124925509

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.