Evidence map›Paper›PMID 27585592›Full record

ArticleGenes & development2016

Loss of the SUMO protease Ulp2 triggers a specific multichromosome aneuploidy.

Hong-Yeoul Ryu, Nicole R Wilson, Sameet Mehta, Soo Seok Hwang, Mark Hochstrasser

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
–field-weighted citation impact
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

38 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  4. Review
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  8. Article
  9. Article
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  11. Histone modification inComputational and structural biotechnology journal · 2023
    Review
  12. Article
  13. Review
  14. SUMOylation and Major Depressive Disorder.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Effects of aneuploidy on cell behaviour and function.Nature reviews. Molecular cell biology · 2022
    Review
  17. Review
  18. Article
  19. Review
  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

5 authors at 1 institution in 1 country.

Hong-Yeoul RyuDepartment of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06520, USA;
Nicole R WilsonDepartment of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06520, USA;
Sameet MehtaYale Center for Genome Analysis, Yale University, New Haven, Connecticut 06520, USA;
Soo Seok HwangDepartment of Immunobiology, Yale University, New Haven, Connecticut 06520, USA.
Mark HochstrasserDepartment of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06520, USA;
Yale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
FUNCTIONS AND MECHANISMS OF DEUBIQUITINATING ENZYMESR01GM053756 · NIGMS · YALE UNIVERSITY · PI HOCHSTRASSER, MARK W · 1996 to 2019
$6.5M
Elucidating the connections between the SUMO pathway and the ER stress responseF31AG046965 · NIA · YALE UNIVERSITY · PI WILSON, NICOLE RENEE · 2013 to 2015
$53k
NCATS NIH HHS UL1 TR001863NIA NIH HHS F31 AG046965NIGMS NIH HHS R01 GM053756
6 · The paper itself

Abstract

Post-translational protein modification by the small ubiquitin-related modifier (SUMO) regulates numerous cellular pathways, including transcription, cell division, and genome maintenance. The SUMO protease Ulp2 modulates many of these SUMO-dependent processes in budding yeast. From whole-genome RNA sequencing (RNA-seq), we unexpectedly discovered that cells lacking Ulp2 display a twofold increase in transcript levels across two particular chromosomes: chromosome I (ChrI) and ChrXII. This is due to the two chromosomes being present at twice their normal copy number. An abnormal number of chromosomes, termed aneuploidy, is usually deleterious. However, development of specific aneuploidies allows rapid adaptation to cellular stresses, and aneuploidy characterizes most human tumors. Extra copies of ChrI and ChrXII appear quickly following loss of active Ulp2 and can be eliminated following reintroduction of ULP2, suggesting that aneuploidy is a reversible adaptive mechanism to counteract loss of the SUMO protease. Importantly, increased dosage of two genes on ChrI-CLN3 and CCR4, encoding a G1-phase cyclin and a subunit of the Ccr4-Not deadenylase complex, respectively-suppresses ulp2Δ aneuploidy, suggesting that increased levels of these genes underlie the aneuploidy induced by Ulp2 loss. Our results reveal a complex aneuploidy mechanism that adapts cells to loss of the SUMO protease Ulp2.

Indexed as

AneuploidyAdaptation, PhysiologicalCell CycleChromosomes, FungalEndopeptidasesGene DeletionGene DosageGene Expression Regulation, FungalGenome, FungalRNA, MessengerSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsEndopeptidasesRNA, MessengerSaccharomyces cerevisiae ProteinsULP2 protein, S cerevisiaeaneuploidyCcr4Cln3proteaseSUMOUlp2

Identifiers

PMID27585592
PMCPMC5024685
OpenAlexW2507829853

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.