Evidence map›Paper›PMID 32857970›Full record

ArticleCurrent biology : CB2020

Synaptic Protein Degradation Controls Sexually Dimorphic Circuits through Regulation of DCC/UNC-40.

Yehuda Salzberg, Vladyslava Pechuk, Asaf Gat, Hagar Setty, Sapir Sela, Meital Oren-Suissa

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Yehuda SalzbergDepartment of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel.
Vladyslava PechukDepartment of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel.
Asaf GatDepartment of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel.
Hagar SettyDepartment of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel.
Sapir SelaDepartment of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel.
Meital Oren-SuissaDepartment of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel. Electronic address: meital.oren@weizmann.ac.il.
Weizmann Institute of Science · IL

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
NIH HHS P40 OD010440
6 · The paper itself

Abstract

Sexually dimorphic circuits underlie behavioral differences between the sexes, yet the molecular mechanisms involved in their formation are poorly understood. We show here that sexually dimorphic connectivity patterns arise in C. elegans through local ubiquitin-mediated protein degradation in selected synapses of one sex but not the other. Specifically, synaptic degradation occurs via binding of the evolutionary conserved E3 ligase SEL-10/FBW7 to a phosphodegron binding site of the netrin receptor UNC-40/DCC (Deleted in Colorectal Cancer), resulting in degradation of UNC-40. In animals carrying an undegradable unc-40 gain-of-function allele, synapses were retained in both sexes, compromising the activity of the circuit without affecting neurite guidance. Thus, by decoupling the synaptic and guidance functions of the netrin pathway, we reveal a critical role for dimorphic protein degradation in controlling neuronal connectivity and activity. Additionally, the interaction between SEL-10 and UNC-40 is necessary not only for sex-specific synapse pruning, but also for other synaptic functions. These findings provide insight into the mechanisms that generate sex-specific differences in neuronal connectivity, activity, and function.

Indexed as

Sex CharacteristicsAllelesAnimalsAnimals, Genetically ModifiedAxonsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell Adhesion MoleculesCell Cycle ProteinsGain of Function MutationMaleProteolysisSynapsesSynaptic TransmissionUbiquitinationCaenorhabditis elegans ProteinsCell Adhesion MoleculesCell Cycle ProteinsSEL-10 protein, C elegansUNC-40 protein, C elegansC. elegansDCC/UNC-40FBW7/SEL-10protein degradationsexual dimorphismsynapse pruningsynaptic connectivityubiquitin-proteasome pathway

Identifiers

PMID32857970
PMCPMC7658809
OpenAlexW3080394826

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.