Evidence map›Paper›PMID 23457234›Full record

ArticleGenetics2013

The SWI/SNF chromatin remodeling complex selectively affects multiple aspects of serotonergic neuron differentiation.

Peter Weinberg, Nuria Flames, Hitoshi Sawa, Gian Garriga, Oliver Hobert

Abstract read
In one paragraph

Article in Genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. The regulatory landscape of neurite development inFrontiers in molecular neuroscience · 2022
    Review
  6. Systemic enhancement of serotonin signaling reverses social deficits in multiple mouse models for ASD.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  7. Article
  8. Review
  9. The BAF complex in development and disease.Epigenetics & chromatin · 2019
    Review
  10. The role of ARID1B, a BAF chromatin remodeling complex subunit, in neural development and behavior.Progress in neuro-psychopharmacology & biological psychiatry · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. The role of BAF (mSWI/SNF) complexes in mammalian neural development.American journal of medical genetics. Part C, Seminars in medical genetics · 2014
    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

5 authors.

Peter WeinbergDepartment of Biochemistry and Molecular Biophysics, Howard Hughes Medical Institute, Columbia University Medical Center, New York, New York 10032, USA.
Nuria Flames
Hitoshi Sawa
Gian Garriga
Oliver Hobert

Funding

LIM HOMEOBOX GENE LIM-6 IN MOTOR NEURON DIFFERENTIATIONR01NS039996 · NINDS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Oliver Hobert · 2001 to 2026
$6.8M
Wnt regulation of C. elegans neuroblast and neuronal polarityR01NS032057 · NINDS · UNIVERSITY OF CALIFORNIA BERKELEY · PI GARRIGA, GIAN · 1994 to 2020
$6.7M
Genetic analysis of dopaminergic neuron specification in C.elegansR01NS050266 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HOBERT, OLIVER · 2004 to 2013
$3.4M
Howard Hughes Medical InstituteNINDS NIH HHS R01 NS032057NINDS NIH HHS R01 NS039996NINDS NIH HHS R01NS039996-05NINDS NIH HHS R01 NS050266NINDS NIH HHS R01NS050266-03
6 · The paper itself

Abstract

Regulatory programs that control the specification of serotonergic neurons have been investigated by genetic mutant screens in the nematode Caenorhabditis elegans. Loss of a previously uncloned gene, ham-3, affects migration and serotonin antibody staining of the hermaphrodite-specific neuron (HSN) pair. We characterize these defects here in more detail, showing that the defects in serotonin antibody staining are paralleled by a loss of the transcription of all genes involved in serotonin synthesis and transport. This loss is specific to the HSN class as other serotonergic neurons appear to differentiate normally in ham-3 null mutants. Besides failing to migrate appropriately, the HSNs also display axon pathfinding defects in ham-3 mutants. However, the HSNs are still generated and express a subset of their terminal differentiation features in ham-3 null mutants, demonstrating that ham-3 is a specific regulator of select features of the HSNs. We show that ham-3 codes for the C. elegans ortholog of human BAF60, Drosophila Bap60, and yeast Swp73/Rsc6, which are subunits of the yeast SWI/SNF and vertebrate BAF chromatin remodeling complex. We show that the effect of ham-3 on serotonergic fate can be explained by ham-3 regulating the expression of the Spalt/SALL-type Zn finger transcription factor sem-4, a previously identified regulator of serotonin expression in HSNs and of the ham-2 Zn transcription factor, a previously identified regulator of HSN migration and axon outgrowth. Our findings provide the first evidence for the involvement of the BAF complex in the acquisition of terminal neuronal identity and constitute genetic proof by germline knockout that a BAF complex component can have cell-type-specific roles during development.

Indexed as

Cell DifferentiationChromatin Assembly and DisassemblyAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell MovementChromosomal Proteins, Non-HistoneGenes, EssentialGenes, HelminthHumansMutationProtein SubunitsSerotonergic NeuronsSerotoninTranscription FactorsCaenorhabditis elegans ProteinsChromosomal Proteins, Non-HistoneProtein SubunitsSerotoninSWI-SNF-B chromatin-remodeling complexTranscription Factors

Identifiers

PMID23457234
PMCPMC3632466

What OpenQuestion holds

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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.