Evidence map›Paper›PMID 24965231›Full record

ArticleStem cells (Dayton, Ohio)2014

Passage number is a major contributor to genomic structural variations in mouse iPSCs.

Pengfei Liu, Anna Kaplan, Bo Yuan, Jacob H Hanna, James R Lupski, Orly Reiner

Abstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed.

  1. The complete genome of the KOLF2.1J reference iPSC line.bioRxiv : the preprint server for biology · 2026
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  5. Article
  6. Article
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  9. Clan genomics: From OMIM phenotypic traits to genes and biology.American journal of medical genetics. Part A · 2021
    Article
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  11. 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

6 authors.

Pengfei LiuDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Anna Kaplan
Bo Yuan
Jacob H Hanna
James R Lupski
Orly Reiner

Funding

ZOLENDRONIC ACID IN CHILDREN W/ SEVERE OSTEOGENESIS IMPERFECTAM01RR000188 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI SHEARER, WILLIAM THOMAS · 1985 to 2011
$30.6M
UNDERSTANDING FXTAS AMONG MALES WITH THE FMR1 PREMUTATIONP30HD024064 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI TOLIAS, KIMBERLY R · 1988 to 2013
$29.4M
Steps towards a paternal gene activation therapy for Angelman syndromeU54HD083092 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI NELSON, DAVID LOREN, NEUL, JEFFREY L · 2014 to 2019
$7.8M
Nonrecurrent rearrangements, genome architecture and neurodegenerative disease.R01NS058529 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI LUPSKI, JAMES R. · 2009 to 2017
$5.0M
NCRR NIH HHS M01 RR000188NCRR NIH HHS M01RR00188NICHD NIH HHS P30 HD024064NICHD NIH HHS P30HD024064NICHD NIH HHS U54 HD083092NINDS NIH HHS R01 NS058529NINDS NIH HHS R01NS058529
6 · The paper itself

Abstract

Emergence of genomic instability is a practical issue in preparing neural stem cells (NSCs) and induced pluripotent stem cells (iPSCs). However, it is still not fully understood what the origins and mechanisms for formation are for the genomic alternations observed. Here, we studied the extent of genomic variation on the scale of individual cells originating from the same animal. We used mouse NSCs grown from embryonic cells and iPSCs generated from embryonic brain cells, B cells or fibroblasts, and performed comparative analysis with cultures of fibroblasts from the same mouse. In the first passage of these cell lines, aneuploidies were only observed for chromosomes 6, 11, 12, 19, and Y, which is overall at a rate lower than previously reported; de novo copy number variations (CNVs) were observed in 4.3% of neural iPSCs, 29% of B cell iPSCs, 10% of fibroblast iPSCs, and 1.3% of neurospheres. In contrast, propagation of these first passage cells to a later passage induced additional aneuploidies and CNVs. Breakpoint sequencing analysis suggested that the majority of the detected CNVs arose by replicative mechanisms. Interestingly, we detected identical de novo CNVs in different single cell colonies that appeared to have arisen independently from each other, which suggests a novel CNV formation mechanism in these cells. Our findings provide insights into mechanisms of CNV formation during reprogramming and suggest that replicative mechanisms for CNV formation accompany mitotic divisions.

Indexed as

Genomic Structural VariationAneuploidyAnimalsBase SequenceCell ProliferationChromosome BreakageClone CellsComparative Genomic HybridizationDNA Copy Number VariationsGenetic LociGenomic InstabilityInduced Pluripotent Stem CellsMiceMolecular Sequence DataNeural Stem CellsSpheroids, CellularChromosomal aberrationsDNA copy number variationsDNA replicationInduced pluripotent stem cellsNeural stem cells

Identifiers

PMID24965231
PMCPMC4165691

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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.