Evidence map›Paper›PMID 36912772›Full record

ArticleThe Journal of cell biology2023

Septin-mediated RhoA activation engages the exocyst complex to recruit the cilium transition zone.

Darya Safavian, Moshe S Kim, Hong Xie, Maha El-Zeiry, Oliva Palander, Lu Dai, Richard F Collins, Carol Froese, Rachel Shannon, Koh-Ichi Nagata and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. bioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. 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

11 authors at 3 institutions in 2 countries.

Darya Safavian *Cell Biology Program, Hospital for Sick Children , Toronto, Ontario, Canada.ORCID 0000-0003-1943-6800
Moshe S Kim *Cell Biology Program, Hospital for Sick Children , Toronto, Ontario, Canada.
Hong XieCell Biology Program, Hospital for Sick Children , Toronto, Ontario, Canada.
Maha El-ZeiryCell Biology Program, Hospital for Sick Children , Toronto, Ontario, Canada.ORCID 0000-0001-5375-105X
Oliva PalanderCell Biology Program, Hospital for Sick Children , Toronto, Ontario, Canada.ORCID 0000-0002-7085-3688
Lu DaiCell Biology Program, Hospital for Sick Children , Toronto, Ontario, Canada.
Richard F CollinsCell Biology Program, Hospital for Sick Children , Toronto, Ontario, Canada.ORCID 0000-0002-0670-7424
Carol FroeseCell Biology Program, Hospital for Sick Children , Toronto, Ontario, Canada.
Rachel ShannonCell Biology Program, Hospital for Sick Children , Toronto, Ontario, Canada.ORCID 0000-0001-9494-5088
Koh-Ichi NagataDepartment of Molecular Neurobiology, Institute for Developmental Research, Aichi Human Service Center , Kasugai, Aichi, Japan.ORCID 0000-0002-6827-8434
William S TrimbleCell Biology Program, Hospital for Sick Children , Toronto, Ontario, Canada.ORCID 0000-0001-9776-5111
Hospital for Sick Children · CAUniversity of Toronto · CAAichi Human Service Center · JP

Funding

CIHR PJT-152194
6 · The paper itself

Abstract

Septins are filamentous GTPases that play important but poorly characterized roles in ciliogenesis. Here, we show that SEPTIN9 regulates RhoA signaling at the base of cilia by binding and activating the RhoA guanine nucleotide exchange factor, ARHGEF18. GTP-RhoA is known to activate the membrane targeting exocyst complex, and suppression of SEPTIN9 causes disruption of ciliogenesis and mislocalization of an exocyst subunit, SEC8. Using basal body-targeted proteins, we show that upregulating RhoA signaling at the cilium can rescue ciliary defects and mislocalization of SEC8 caused by global SEPTIN9 depletion. Moreover, we demonstrate that the transition zone components, RPGRIP1L and TCTN2, fail to accumulate at the transition zone in cells lacking SEPTIN9 or depleted of the exocyst complex. Thus, SEPTIN9 regulates the recruitment of transition zone proteins on Golgi-derived vesicles by activating the exocyst via RhoA to allow the formation of primary cilia.

Indexed as

CiliarhoA GTP-Binding ProteinSeptinsCytoplasmGuanine Nucleotide Exchange FactorsSignal TransductionGuanine Nucleotide Exchange FactorsrhoA GTP-Binding ProteinSeptins

Identifiers

PMID36912772
PMCPMC10039714
OpenAlexW4324018425

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.