Evidence map›Paper›PMID 22090492›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Serum response factor is required for cortical axon growth but is dispensable for neurogenesis and neocortical lamination.

Paul P Y Lu, Narendrakumar Ramanan

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  15. Article
  16. SRF phosphorylation by glycogen synthase kinase-3 promotes axon growth in hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  17. Article
  18. The transcription factor serum response factor stimulates axon regeneration through cytoplasmic localization and cofilin interaction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  19. Article
  20. A critical cell-intrinsic role for serum response factor in glial specification in the CNS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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

2 authors at 1 institution in 1 country.

Paul P Y LuDepartment of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Narendrakumar Ramanan
Washington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have shown that neuron-specific deletion of serum response factor (SRF) results in deficits in tangential cell migration, guidance-dependent circuit assembly, activity-dependent gene expression, and synaptic plasticity in the hippocampus. Furthermore, SRF deletion in mouse embryonic stem cells causes cell death in vitro. However, the requirement of SRF for early neuronal development including neural stem cell homeostasis, neurogenesis, and axonal innervations remains unknown. Here, we report that SRF is critical for development of major axonal tracts in the forebrain. Conditional mutant mice lacking SRF in neural progenitor cells (Srf-Nestin-cKO) exhibit striking deficits in cortical axonal projections including corticostriatal, corticospinal, and corticothalamic tracts, and they show a variable loss of the corpus callosum. Neurogenesis and interneuron specification occur normally in the absence of SRF and the deficits in axonal projections were not due to a decrease or loss in cell numbers. Radial migration of neurons and neocortical lamination were also not affected. No aberrant cell death was observed during development, whereas there was an increase in the number of proliferative cells in the ventricular zone from embryonic day 14 to day 18. Similar axonal tract deficits were also observed in mutant mice lacking SRF in the developing excitatory neurons of neocortex and hippocampus (Srf-NEX-cKO). Together, these findings suggest distinct roles for SRF during neuronal development; SRF is specifically required in a cell-autonomous manner for axonal tract development but is dispensable for cell survival, neurogenesis, neocortical lamination, and neuronal differentiation.

Indexed as

Age FactorsAmino AcidsAnimalsAnimals, Genetically ModifiedAnimals, NewbornAxonsCaspase 3Cell CountEmbryo, MammalianGene Expression Regulation, DevelopmentalIn Situ Nick-End LabelingIntermediate Filament ProteinsMiceMutationNeocortexNerve Tissue ProteinsAmino AcidsCaspase 3dolaisoleucineEomes protein, mouseIntermediate Filament ProteinsNerve Tissue ProteinsNes protein, mouseNestinSerum Response FactorT-Box Domain Proteins

Identifiers

PMID22090492
PMCPMC6633287
OpenAlexW2012071465

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.