Evidence map›Paper›PMID 21284845›Full record

ArticleNeural development2011

The chromatin remodeling factor Bap55 functions through the TIP60 complex to regulate olfactory projection neuron dendrite targeting.

Joy S Tea, Liqun Luo

Open access · goldAbstract read
In one paragraph

Article in Neural development, 2011. 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
3.1field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  7. Investigating Developmental and Epileptic Encephalopathy UsingInternational journal of molecular sciences · 2020
    Review
  8. Loss of the neural-specific BAF subunit ACTL6B relieves repression of early response genes and causes recessive autism.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Article
  10. The True Story ofFrontiers in physiology · 2019
    Review
  11. Article
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  18. The role of BAF (mSWI/SNF) complexes in mammalian neural development.American journal of medical genetics. Part C, Seminars in medical genetics · 2014
    Article
  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

2 authors at 2 institutions in 1 country.

Joy S TeaHoward Hughes Medical Institute, Department of Biology, Stanford University, Stanford, CA 94305, USA.
Liqun Luo
Howard Hughes Medical Institute · USStanford University · US

Funding

Assembly of the Central Olfactory Networks in DrosophilaR01DC005982 · NIDCD · STANFORD UNIVERSITY · PI LIQUN LUO · 2003 to 2026
$8.1M
Howard Hughes Medical InstituteNIDCD NIH HHS R01-DC005982
6 · The paper itself

Abstract

backgroundThe Drosophila olfactory system exhibits very precise and stereotyped wiring that is specified predominantly by genetic programming. Dendrites of olfactory projection neurons (PNs) pattern the developing antennal lobe before olfactory receptor neuron axon arrival, indicating an intrinsic wiring mechanism for PN dendrites. These wiring decisions are likely determined through a transcriptional program.

resultsWe find that loss of Brahma associated protein 55 kD (Bap55) results in a highly specific PN mistargeting phenotype. In Bap55 mutants, PNs that normally target to the DL1 glomerulus mistarget to the DA4l glomerulus with 100% penetrance. Loss of Bap55 also causes derepression of a GAL4 whose expression is normally restricted to a small subset of PNs. Bap55 is a member of both the Brahma (BRM) and the Tat interactive protein 60 kD (TIP60) ATP-dependent chromatin remodeling complexes. The Bap55 mutant phenotype is partially recapitulated by Domino and Enhancer of Polycomb mutants, members of the TIP60 complex. However, distinct phenotypes are seen in Brahma and Snf5-related 1 mutants, members of the BRM complex. The Bap55 mutant phenotype can be rescued by postmitotic expression of Bap55, or its human homologs BAF53a and BAF53b.

conclusionsOur results suggest that Bap55 functions through the TIP60 chromatin remodeling complex to regulate dendrite wiring specificity in PNs. The specificity of the mutant phenotypes suggests a position for the TIP60 complex at the top of a regulatory hierarchy that orchestrates dendrite targeting decisions.

Indexed as

ActinsAnimalsAnimals, Genetically ModifiedChromosomal Proteins, Non-HistoneDendritesDNA-Binding ProteinsDrosophilaDrosophila ProteinsGene Expression RegulationHistone AcetyltransferasesHumansMushroom BodiesMutationNeuronsOlfactory PathwaysPhenotypeActinsACTL6A protein, humanChromosomal Proteins, Non-HistoneDNA-Binding Proteinsdom protein, DrosophilaDrosophila ProteinsHistone AcetyltransferasesSMARCB1 ProteinSMARCB1 protein, humanTip60 protein, DrosophilaTranscription Factors

Identifiers

PMID21284845
PMCPMC3038883
OpenAlexW2028653421

What OpenQuestion holds

Textmetadata
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.