Evidence map›Paper›PMID 31932607›Full record

ArticleNature communications2020

Spatially and temporally defined lysosomal leakage facilitates mitotic chromosome segregation.

Saara Hämälistö, Jonathan Lucien Stahl, Elena Favaro, Qing Yang, Bin Liu, Line Christoffersen, Ben Loos, Claudia Guasch Boldú, Johanna A Joyce, Thomas Reinheckel and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 79 citations in OpenAlex.

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  11. Lysosomes' fallback strategies: more than just survival or death.Frontiers in cell and developmental biology · 2025
    Review
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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

12 authors at 5 institutions in 4 countries.

Saara HämälistöCell Death and Metabolism, Center for Autophagy, Recycling and Disease, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark.
Jonathan Lucien StahlCell Death and Metabolism, Center for Autophagy, Recycling and Disease, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-9476-5455
Elena FavaroCell Death and Metabolism, Center for Autophagy, Recycling and Disease, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark.
Qing YangCell Death and Metabolism, Center for Autophagy, Recycling and Disease, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-3128-8620
Bin LiuCell Death and Metabolism, Center for Autophagy, Recycling and Disease, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark.ORCID http://orcid.org/0000-0001-7489-9125
Line ChristoffersenCell Death and Metabolism, Center for Autophagy, Recycling and Disease, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark.
Ben LoosDepartment of Physiological Sciences, Stellenbosch University, 7600, Stellenbosch, South Africa.ORCID http://orcid.org/0000-0002-5517-373X
Claudia Guasch BoldúCell Division and Cytoskeleton, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark.
Johanna A JoyceLudwig Institute for Cancer Research, University of Lausanne, 1005, Lausanne, Switzerland.ORCID http://orcid.org/0000-0002-6332-2598
Thomas ReinheckelInstitute of Molecular Medicine and Cell Research, Medical Faculty, University of Freiburg, 79104, Freiburg, Germany.ORCID http://orcid.org/0000-0001-9866-9105
Marin BarisicCell Division and Cytoskeleton, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark.ORCID http://orcid.org/0000-0001-7587-3867
Marja JäätteläCell Death and Metabolism, Center for Autophagy, Recycling and Disease, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark. mj@cancer.dk.ORCID http://orcid.org/0000-0001-5950-7111
Danish Cancer Society · DKUniversity of Copenhagen · DKLudwig Cancer Research · CHStellenbosch University · ZAUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysosomes are membrane-surrounded cytoplasmic organelles filled with a powerful cocktail of hydrolases. Besides degrading cellular constituents inside the lysosomal lumen, lysosomal hydrolases promote tissue remodeling when delivered to the extracellular space and cell death when released to the cytosol. Here, we show that spatially and temporally controlled lysosomal leakage contributes to the accurate chromosome segregation in normal mammalian cell division. One or more chromatin-proximal lysosomes leak in the majority of prometaphases, after which active cathepsin B (CTSB) localizes to the metaphase chromatin and cleaves a small subset of histone H3. Stabilization of lysosomal membranes or inhibition of CTSB activity during mitotic entry results in a significant increase in telomere-related chromosome segregation defects, whereas cells and tissues lacking CTSB and cells expressing CTSB-resistant histone H3 accumulate micronuclei and other nuclear defects. These data suggest that lysosomal leakage and chromatin-associated CTSB contribute to proper chromosome segregation and maintenance of genomic integrity.

Indexed as

Chromosome SegregationMitosisAnimalsCathepsin BCell LineCell NucleusChromatinFemaleGene SilencingHistonesHumansIntracellular MembranesLysosomesMetaphaseMicePermeabilityCathepsin BChromatinHistones

Identifiers

PMID31932607
PMCPMC6957743
OpenAlexW2998839829

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.