Evidence map›Paper›PMID 25456499›Full record

ArticleNeuron2014

MST3 kinase phosphorylates TAO1/2 to enable Myosin Va function in promoting spine synapse development.

Sila K Ultanir, Smita Yadav, Nicholas T Hertz, Juan A Oses-Prieto, Suzanne Claxton, Alma L Burlingame, Kevan M Shokat, Lily Y Jan, Yuh-Nung Jan

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuron, 2014. 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
1.5field-weighted citation impact, top 19% 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, 79 citations in OpenAlex.

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  18. Ste20-like Kinase Is Critical for Inhibitory Synapse Maintenance and Its Deficiency Confers a Developmental Dendritopathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
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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

9 authors at 3 institutions in 2 countries.

Sila K UltanirDepartments of Physiology, Biochemistry, and Biophysics, University of California, San Francisco, San Francisco, CA 94158, USA; Medical Research Council, National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK. Electronic address: sila.ultanir@nimr.mrc.ac.uk.
Smita YadavDepartments of Physiology, Biochemistry, and Biophysics, University of California, San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158, USA.
Nicholas T HertzDepartment of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158, USA.
Juan A Oses-PrietoDepartment of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, CA 94158, USA.
Suzanne ClaxtonMedical Research Council, National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK.
Alma L BurlingameDepartment of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, CA 94158, USA.
Kevan M ShokatDepartment of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158, USA.
Lily Y JanDepartments of Physiology, Biochemistry, and Biophysics, University of California, San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158, USA.
Yuh-Nung JanDepartments of Physiology, Biochemistry, and Biophysics, University of California, San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: yuhnung.jan@ucsf.edu.
University of California, San Francisco · USHoward Hughes Medical Institute · USMedical Research Council · GB

Funding

RESEARCH TRAINING IN CHEMISTRY AND CHEMICAL BIOLOGYT32GM064337 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CRAIK, CHARLES SCOTT · 2002 to 2021
$7.8M
Bio-Organic Biomedical Mass Spectromy ResourceP41GM103481 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BURLINGAME, ALMA L · 2012 to 2015
$6.4M
Using chemical genetics to investigate mechanisms of anesthetic actionR01EB001987 · NIBIB · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHOKAT, KEVAN M. · 2003 to 2012
$2.9M
Genetic Dissection of Dendrite DevelopmentR37NS040929 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JAN, YUH NUNG · 2010 to 2016
$2.5M
Molecular mechanisms of dendrite development in mammalian CNSR01MH084234 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JAN, YUH NUNG · 2008 to 2012
$1.7M
Howard Hughes Medical InstituteMedical Research Council MC_UP_1202/6NIBIB NIH HHS R01 EB001987NIBIB NIH HHS R01EB001987NIGMS NIH HHS 8P41GM103481NIGMS NIH HHS P41 GM103481NIGMS NIH HHS T32 GM064337NIMH NIH HHS 5R01MH084234NIMH NIH HHS R01 MH084234NINDS NIH HHS R37 NS040929NINDS NIH HHS R37NS040929
6 · The paper itself

Abstract

Mammalian Sterile 20 (Ste20)-like kinase 3 (MST3) is a ubiquitously expressed kinase capable of enhancing axon outgrowth. Whether and how MST3 kinase signaling might regulate development of dendritic filopodia and spine synapses is unknown. Through shRNA-mediated depletion of MST3 and kinase-dead MST3 expression in developing hippocampal cultures, we found that MST3 is necessary for proper filopodia, dendritic spine, and excitatory synapse development. Knockdown of MST3 in layer 2/3 pyramidal neurons via in utero electroporation also reduced spine density in vivo. Using chemical genetics, we discovered thirteen candidate MST3 substrates and identified the phosphorylation sites. Among the identified MST3 substrates, TAO kinases regulate dendritic filopodia and spine development, similar to MST3. Furthermore, using stable isotope labeling by amino acids in culture (SILAC), we show that phosphorylated TAO1/2 associates with Myosin Va and is necessary for its dendritic localization, thus revealing a mechanism for excitatory synapse development in the mammalian CNS.

Indexed as

Age FactorsAnimalsCells, CulturedDendritic SpinesEmbryo, MammalianGene Expression Regulation, DevelopmentalHippocampusHippo KinasesHumansMAP Kinase Kinase KinasesMicrotubule-Associated ProteinsMutationMyosin Heavy ChainsMyosin Type VNeuronsPhosphorylationHippo KinasesMAP2 protein, ratMAP Kinase Kinase KinasesMicrotubule-Associated ProteinsMyo5a protein, ratMyosin Heavy ChainsMyosin Type VProtein Serine-Threonine KinasesRNA, Small InterferingSTK24 protein, humanTAO1 protein kinaseTaok2 protein, rat

Identifiers

PMID25456499
PMCPMC4407996
OpenAlexW2073203830

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.