Evidence map›Paper›PMID 29243212›Full record

ReviewChromosoma2018

Controlling centriole numbers: Geminin family members as master regulators of centriole amplification and multiciliogenesis.

Marina Arbi, Dafni-Eleftheria Pefani, Stavros Taraviras, Zoi Lygerou

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Chromosoma, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

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  6. The Crk4-Cyc4 complex regulates GThe EMBO journal · 2024
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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

4 authors at 1 institution in 2 countries.

Marina ArbiLaboratory of Biology, School of Medicine, University of Patras, 26504 Rio, Patras, Greece.
Dafni-Eleftheria PefaniLaboratory of Biology, School of Medicine, University of Patras, 26504 Rio, Patras, Greece.
Stavros TaravirasLaboratory of Physiology, School of Medicine, University of Patras, 26504 Rio, Patras, Greece.
Zoi LygerouLaboratory of Biology, School of Medicine, University of Patras, 26504 Rio, Patras, Greece. lygerou@med.upatras.gr.ORCID 0000-0001-5683-0220
University of Patras · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To ensure that the genetic material is accurately passed down to daughter cells during mitosis, dividing cells must duplicate their chromosomes and centrosomes once and only once per cell cycle. The same key steps-licensing, duplication, and segregation-control both the chromosome and the centrosome cycle, which must occur in concert to safeguard genome integrity. Aberrations in genome content or centrosome numbers lead to genomic instability and are linked to tumorigenesis. Such aberrations, however, can also be part of the normal life cycle of specific cell types. Multiciliated cells best exemplify the deviation from a normal centrosome cycle. They are post-mitotic cells which massively amplify their centrioles, bypassing the rule for once-per-cell-cycle centriole duplication. Hundreds of centrioles dock to the apical cell surface and generate motile cilia, whose concerted movement ensures fluid flow across epithelia. The early steps that control the generation of multiciliated cells have lately started to be elucidated. Geminin and the vertebrate-specific GemC1 and McIdas are distantly related coiled-coil proteins, initially identified as cell cycle regulators associated with the chromosome cycle. Geminin is required to ensure once-per-cell-cycle genome replication, while McIdas and GemC1 bind to Geminin and are implicated in DNA replication control. Recent findings highlight Geminin family members as early regulators of multiciliogenesis. GemC1 and McIdas specify the multiciliate cell fate by forming complexes with the E2F4/5 transcription factors to switch on a gene expression program leading to centriole amplification and cilia formation. Positive and negative interactions among Geminin family members may link cell cycle control to centriole amplification and multiciliogenesis, acting close to the point of transition from proliferation to differentiation. We review key steps of centrosome duplication and amplification, present the role of Geminin family members in the centrosome and chromosome cycle, and discuss links with disease.

Indexed as

GenomeMitosisAnimalsCarcinogenesisCarrier ProteinsCell Cycle ProteinsCentriolesCiliaDNA ReplicationDwarfismE2F4 Transcription FactorE2F5 Transcription FactorGemininGene Expression RegulationGenomic InstabilityHumansCarrier ProteinsCell Cycle ProteinsE2F4 protein, humanE2F4 Transcription FactorE2F5 protein, humanE2F5 Transcription FactorGemininGMNC protein, humanGMNN protein, humanMCIDAS protein, humanNuclear ProteinsTranscription FactorsGemC1GemininGMNCGMNNIdasLynkeasMcIdasMulticilin

Identifiers

PMID29243212
OpenAlexW2775595987

What OpenQuestion holds

Textmetadata
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.