Evidence map›Paper›PMID 31239441›Full record

ArticleNature communications2019

Lzts1 controls both neuronal delamination and outer radial glial-like cell generation during mammalian cerebral development.

T Kawaue, A Shitamukai, A Nagasaka, Y Tsunekawa, T Shinoda, K Saito, R Terada, M Bilgic, T Miyata, F Matsuzaki and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. 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
2.5field-weighted citation impact, top 10% 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, 48 citations in OpenAlex.

  1. Fine-tuning neuron number:bioRxiv : the preprint server for biology · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Unveiling the oncogenic role of LZTS1 in colorectal cancer.Journal of cellular and molecular medicine · 2024
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
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  17. How neural stem cells contribute to neocortex development.Biochemical Society transactions · 2021
    Review
  18. Article
  19. Article
  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

11 authors at 5 institutions in 2 countries.

T KawaueDepartment of Anatomy and Cell Biology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
A ShitamukaiLaboratory for Cell Asymmetry, RIKEN Center for Biosystems Dynamics Research, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.ORCID http://orcid.org/0000-0003-4216-927X
A NagasakaDepartment of Anatomy and Cell Biology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Y TsunekawaLaboratory for Cell Asymmetry, RIKEN Center for Biosystems Dynamics Research, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
T ShinodaDepartment of Anatomy and Cell Biology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
K SaitoDepartment of Anatomy and Cell Biology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
R TeradaDepartment of Anatomy and Cell Biology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
M BilgicLaboratory for Cell Asymmetry, RIKEN Center for Biosystems Dynamics Research, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
T MiyataDepartment of Anatomy and Cell Biology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, Aichi, 466-8550, Japan.ORCID http://orcid.org/0000-0002-5952-0241
F MatsuzakiLaboratory for Cell Asymmetry, RIKEN Center for Biosystems Dynamics Research, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.ORCID http://orcid.org/0000-0001-7902-4520
A KawaguchiDepartment of Anatomy and Cell Biology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, Aichi, 466-8550, Japan. akawa@med.nagoya-u.ac.jp.ORCID http://orcid.org/0000-0002-0339-3992
Nagoya University · JPKyoto University · JPRIKEN Center for Biosystems Dynamics Research · JPMeikai University · JPNational University of Singapore · SG

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) JP16K06990MEXT | Japan Society for the Promotion of Science (JSPS) JP17H05765
6 · The paper itself

Abstract

In the developing central nervous system, cell departure from the apical surface is the initial and fundamental step to form the 3D, organized architecture. Both delamination of differentiating cells and repositioning of progenitors to generate outer radial glial cells (oRGs) contribute to mammalian neocortical expansion; however, a comprehensive understanding of their mechanisms is lacking. Here, we demonstrate that Lzts1, a molecule associated with microtubule components, promotes both cell departure events. In neuronally committed cells, Lzts1 functions in apical delamination by altering apical junctional organization. In apical RGs (aRGs), Lzts1 expression is variable, depending on Hes1 expression levels. According to its differential levels, Lzts1 induces diverse RG behaviors: planar division, oblique divisions of aRGs that generate oRGs, and their mitotic somal translocation. Loss-of-function of lzts1 impairs all these cell departure processes. Thus, Lzts1 functions as a master modulator of cellular dynamics, contributing to increasing complexity of the cerebral architecture during evolution.

Indexed as

NeurogenesisAnimalsCell MovementCerebrumEpendymoglial CellsMiceMice, TransgenicNeuronsTranscription Factor HES-1Tumor Suppressor ProteinsHes1 protein, mouseLzts1 protein, mouseTranscription Factor HES-1Tumor Suppressor Proteins

Identifiers

PMID31239441
PMCPMC6592889
OpenAlexW2955822479

What OpenQuestion holds

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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.