Evidence map›Paper›PMID 27141053›Full record

ArticleMolecular and cellular biology2016

Noncoding Transcription Is a Driving Force for Nucleosome Instability in spt16 Mutant Cells.

Jianxun Feng, Haiyun Gan, Matthew L Eaton, Hui Zhou, Shuqi Li, Jason A Belsky, David M MacAlpine, Zhiguo Zhang, Qing Li

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

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  20. Structure and function of the histone chaperone FACT - Resolving FACTual issues.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018
    Review
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

9 authors at 5 institutions in 2 countries.

Jianxun FengState Key Laboratory of Protein and Plant Gene Research, School of Life Sciences and Peking-Tsinghua Center for Life Sciences, Peking University, Beijing, China Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, China.
Haiyun GanDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Matthew L EatonDepartment of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina, USA.
Hui ZhouDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Shuqi LiAcademy for Advanced Interdisciplinary Studies, Peking University, Beijing, China.
Jason A BelskyDepartment of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina, USA.
David M MacAlpineDepartment of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina, USA.
Zhiguo ZhangDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA Zhang.Zhiguo@mayo.edu li.qing@pku.edu.cn.
Qing LiState Key Laboratory of Protein and Plant Gene Research, School of Life Sciences and Peking-Tsinghua Center for Life Sciences, Peking University, Beijing, China Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, China Zhang.Zhiguo@mayo.edu li.qing@pku.edu.cn.
Mayo Clinic · USDuke Medical Center · USPeking University · CNCenter for Life Sciences · CNDuke University Hospital · US

Funding

Computational Biology and Bioinformatics Training ProgramT32GM071340 · NIGMS · DUKE UNIVERSITY · PI MAGWENE, PAUL MITAARI · 2005 to 2020
$3.3M
Regulation of Nucleosome AssemblyR01GM081838 · NIGMS · MAYO CLINIC ROCHESTER · PI ZHANG, ZHIGUO · 2008 to 2015
$2.4M
Chromatin architecture defines DNA replication originsR01GM104097 · NIGMS · DUKE UNIVERSITY · PI MACALPINE, DAVID M · 2013 to 2016
$1.2M
NIGMS NIH HHS R01 GM081838NIGMS NIH HHS R01 GM104097NIGMS NIH HHS T32 GM071340
6 · The paper itself

Abstract

FACT (facilitates chromatin transcription) consists of two essential subunits, Spt16 and Pob3, and functions as a histone chaperone. Mutation of spt16 results in a global loss of nucleosomes as well as aberrant transcription. Here, we show that the majority of nucleosome changes upon Spt16 depletion are alterations in nucleosome fuzziness and position shift. Most nucleosomal changes are suppressed by the inhibition of RNA polymerase II (Pol II) activity. Surprisingly, a small subgroup of nucleosome changes is resistant to transcriptional inhibition. Notably, Spt16 and distinct histone modifications are enriched at this subgroup of nucleosomes. We also report 1,037 Spt16-suppressed noncoding transcripts (SNTs) and found that the SNT start sites are enriched with the subgroup of nucleosomes resistant to Pol II inhibition. Finally, the nucleosomes at genes overlapping SNTs are more susceptible to changes upon Spt16 depletion than those without SNTs. Taken together, our results support a model in which Spt16 has a role in maintaining local nucleosome stability to inhibit initiation of SNT transcription, which once initiated drives additional nucleosome loss upon Spt16 depletion.

Indexed as

MutationNucleosomesRNA Polymerase IISaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranscriptional Elongation FactorsTranscription, GeneticNucleosomesRNA Polymerase IISaccharomyces cerevisiae ProteinsSPT16 protein, S cerevisiaeTranscriptional Elongation Factors

Identifiers

PMID27141053
PMCPMC4911744
OpenAlexW2347201600

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.