Evidence map›Paper›PMID 26400094›Full record

ArticleDevelopment (Cambridge, England)2015

Tracking and transforming neocortical progenitors by CRISPR/Cas9 gene targeting and piggyBac transposase lineage labeling.

Fuyi Chen, Joel Rosiene, Alicia Che, Albert Becker, Joseph LoTurco

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Advances in CRISPR-Cas9 in lineage tracing of model animals.Animal models and experimental medicine · 2025
    Review
  3. Review
  4. Review
  5. Article
  6. The mTOR pathway genesbioRxiv : the preprint server for biology · 2024
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. CRISPR/Cas-Dependent and Nuclease-FreeHuman gene therapy · 2021
    Review
  19. Article
  20. 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

5 authors at 3 institutions in 2 countries.

Fuyi ChenDepartment of Physiology and Neurobiology, Institute for Systems Genomics, Institute for Brain and Cognitive Science, University of Connecticut, Storrs, CT 06268, USA.
Joel RosieneDepartment of Physiology and Neurobiology, Institute for Systems Genomics, Institute for Brain and Cognitive Science, University of Connecticut, Storrs, CT 06268, USA.
Alicia CheDepartment of Physiology and Neurobiology, Institute for Systems Genomics, Institute for Brain and Cognitive Science, University of Connecticut, Storrs, CT 06268, USA.
Albert BeckerDepartment of Neuropathology, University of Bonn Medical Center, 53105 Born, Germany.
Joseph LoTurcoDepartment of Physiology and Neurobiology, Institute for Systems Genomics, Institute for Brain and Cognitive Science, University of Connecticut, Storrs, CT 06268, USA Joseph.loturco@uconn.edu.
Institute for Systems Biology · USUniversity of Connecticut · USUniversity of Bonn · DE

Funding

MOLECULAR REGULATION OF NEOCORTICAL NEUROGENESISR01MH056524 · NIMH · UNIVERSITY OF CONNECTICUT STORRS · PI LOTURCO, JOSEPH J · 2003 to 2012
$3.3M
DYSLEXIA SUSCEPTIBILITY GENES AND MECHANISMS OF NEURONAL DEVELOPMENTR01HD055655 · NICHD · UNIVERSITY OF CONNECTICUT STORRS · PI LOTURCO, JOSEPH J · 2008 to 2012
$1.6M
NICHD NIH HHS R01 HD055655NICHD NIH HHS R01HD055655NIMH NIH HHS R01 MH056524NIMH NIH HHS R01MH056524
6 · The paper itself

Abstract

The ability to induce targeted mutations in somatic cells in developing organisms and then track the fates of those cells is a powerful approach both for studying neural development and for modeling human disease. The CRISPR/Cas9 system allows for such targeted mutagenesis, and we therefore tested it in combination with a piggyBac transposase lineage labeling system to track the development of neocortical neural progenitors with targeted mutations in genes linked to neurodevelopmental disruptions and tumor formation. We show that sgRNAs designed to target PTEN successfully decreased PTEN expression, and led to neuronal hypertrophy and altered neuronal excitability. Targeting NF1, by contrast, caused increased astrocytogenesis at the expense of neurogenesis, and combined targeting of three tumor suppressors (PTEN, NF1 and P53) resulted in formation of glioblastoma tumors. Our results demonstrate that CRISPR/Cas9 combined with piggyBac transposase lineage labeling can produce unique models of neurodevelopmental disruption and tumors caused by somatic mutation in neural progenitors.

Indexed as

Chromosomes, Artificial, BacterialAnimalsAstrocytesBrainBrain NeoplasmsCell LineageCRISPR-Cas SystemsElectroporationFemaleGlioblastomaHumansMutagenesisMutationNeurofibromin 1NeuronsPregnancyNeurofibromin 1PTEN PhosphohydrolaseTransposasesTumor Suppressor Protein p53CRISPR/Cas9Glioblastoma multiformeIn utero electroporationLineageNeural progenitorspiggyBac

Identifiers

PMID26400094
PMCPMC4631763
OpenAlexW2218878453

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.