Evidence map›Paper›PMID 26150102›Full record

ArticleScientific reports2015

BBS4 and BBS5 show functional redundancy in the BBSome to regulate the degradative sorting of ciliary sensory receptors.

Qingwen Xu, Yuxia Zhang, Qing Wei, Yan Huang, Yan Li, Kun Ling, Jinghua Hu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 80 citations in OpenAlex.

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  14. WGS Revealed NovelInternational journal of molecular sciences · 2023
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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

7 authors at 2 institutions in 1 country.

Qingwen XuDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA.
Yuxia Zhang1] Department of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA [2] Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA.
Qing Wei1] Department of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA [2] Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA.
Yan HuangDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA.
Yan Li1] Department of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA [2] Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA.
Kun LingDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA.
Jinghua Hu1] Department of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA [2] Mayo Translational PKD Center [3] Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA.
Mayo Clinic · USWinnMed · US

Funding

PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI GREGORY J. GORES · 2009 to 2026
$22.2M
Pilot and FeasibilityP30DK090728 · NIDDK · MAYO CLINIC ROCHESTER · PI ROMERO, MICHAEL F. · 2010 to 2019
$11.8M
Research BaseP30DK090868 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI WATNICK, TERRY J · 2010 to 2019
$11.1M
Molecular dissection of the ciliary gateR01DK099160 · NIDDK · MAYO CLINIC ROCHESTER · PI Jinghua Hu · 2014 to 2026
$4.0M
Exploration of the functions of the ciliopathy Arls in cilia.R01DK090038 · NIDDK · MAYO CLINIC ROCHESTER · PI HU, JINGHUA · 2011 to 2019
$3.1M
Phosphoinsitide signaling in Breast Epithelial Morphogenesis and MetastasisR01CA149039 · NCI · MAYO CLINIC ROCHESTER · PI LING, KUN · 2010 to 2014
$1.6M
NCI NIH HHS 1R01CA149039-01A1NCI NIH HHS R01 CA149039NIDDK NIH HHS 1R01DK090038NIDDK NIH HHS 1R01DK099160-01A1NIDDK NIH HHS P30 DK084567NIDDK NIH HHS P30 DK090728NIDDK NIH HHS P30 DK090868NIDDK NIH HHS P30DK90728NIDDK NIH HHS R01 DK090038NIDDK NIH HHS R01 DK099160
6 · The paper itself

Abstract

Cilia harbor sensory receptors for various signaling cascades critical for vertebrate development. However, the mechanisms underlying the ciliary homeostasis of sensory receptors remain elusive. Here, we demonstrate that BBS-4 and BBS-5, two distinct BBSome components, show unexpected functional redundancy in the context of cilia in C. elegans. BBS-4 directly interacts with BBS-5 and the interaction can be disrupted by a conserved mutation identified in human BBS4. Surprisingly, we found that BBS-4 and BBS-5 act redundantly in the BBSome to regulate the ciliary removal, rather than the ciliary entry or retrograde IFT transport, of various sensory receptors. Further analyses indicate that co-depletion of BBS-4 and BBS-5 disrupts the lysosome-targeted degradative sorting of ciliary sensory receptors. Moreover, mammalian BBS4 and BBS5 also interact directly and coordinate the ciliary removal of polycystin 2. Hence, we reveal a novel and highly conserved role for the BBSome in fine-tuning ciliary signaling by regulating the ciliary removal of sensory receptors for lysosomal degradation.

Indexed as

AnimalsBardet-Biedl SyndromeCaenorhabditis elegansCaenorhabditis elegans ProteinsCell LineCiliaCytoskeletal ProteinsDown-RegulationHEK293 CellsHumansMicrotubule-Associated ProteinsMutation, MissensePhosphate-Binding ProteinsProteinsRNA InterferenceRNA, Small InterferingBBS4 protein, humanBBS5 protein, humanCaenorhabditis elegans ProteinsCytoskeletal ProteinsMicrotubule-Associated ProteinsPhosphate-Binding ProteinsProteinsRNA, Small Interfering

Identifiers

PMID26150102
PMCPMC4493597
OpenAlexW807932216

What OpenQuestion holds

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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.