Evidence map›Paper›PMID 32640224›Full record

ArticleCell reports2020

Cyclin N-Terminal Domain-Containing-1 Coordinates Meiotic Crossover Formation with Cell-Cycle Progression in a Cyclin-Independent Manner.

Stephen Gray, Emerson R Santiago, Joshua S Chappie, Paula E Cohen

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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  9. RNF212B E3 ligase is essential for crossover designation and maturation during male and female meiosis in the mouse.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  18. Robust designation of meiotic crossover sites by CDK-2 through phosphorylation of the MutSγ complex.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  19. Cyclins and CDKs in the regulation of meiosis-specific events.Frontiers in cell and developmental biology · 2022
    Review
  20. 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

4 authors at 1 institution in 1 country.

Stephen GrayDepartment of Biomedical Sciences and Center for Reproductive Genomics, Cornell University, Ithaca, NY 14853, USA. Electronic address: stephen.gray@nottingham.ac.uk.
Emerson R SantiagoDepartment of Molecular Medicine, Cornell University, Ithaca, NY 14853, USA.
Joshua S ChappieDepartment of Molecular Medicine, Cornell University, Ithaca, NY 14853, USA.
Paula E CohenDepartment of Biomedical Sciences and Center for Reproductive Genomics, Cornell University, Ithaca, NY 14853, USA. Electronic address: paula.cohen@cornell.edu.
Cornell University · US

Funding

The MLH1-MLH3 Heterodimer in Mammalian Meiotic Recombination and GameogenesisR01HD041012 · NICHD · YESHIVA UNIVERSITY · PI Paula Elaine Cohen · 2003 to 2026
$7.9M
SLX4 as a mediator of crossover pathway decisions in mammalian meiosisR01HD097987 · NICHD · CORNELL UNIVERSITY · PI COHEN, PAULA ELAINE · 2019 to 2023
$1.9M
Temporal regulation of prophase I events by the cyclin-dependent kinases (CDKs) 2 and 4 in mammalian meiosisK99HD092618 · NICHD · CORNELL UNIVERSITY · PI GRAY, STEPHEN · 2017 to 2018
$202k
NICHD NIH HHS K99 HD092618NICHD NIH HHS R01 HD041012NICHD NIH HHS R01 HD097987
6 · The paper itself

Abstract

During mammalian meiotic prophase I, programmed DNA double-strand breaks are repaired by non-crossover or crossover events, the latter predominantly occurring via the class I crossover pathway and requiring the cyclin N-terminal domain-containing 1(CNTD1) protein. Using an epitope-tagged Cntd1 allele, we detect a short isoform of CNTD1 in vivo that lacks a predicted N-terminal cyclin domain and does not bind cyclin-dependent kinases. Instead, we find that the short-form CNTD1 variant associates with components of the replication factor C (RFC) machinery to facilitate crossover formation, and with the E2 ubiquitin conjugating enzyme, CDC34, to regulate ubiquitylation and subsequent degradation of the WEE1 kinase, thereby modulating cell-cycle progression. We propose that these interactions facilitate a role for CNTD1 as a stop-go regulator during prophase I, ensuring accurate and complete crossover formation before allowing metaphase progression and the first meiotic division.

Indexed as

Crossing Over, GeneticMeiosisAllelesAnimalsCell NucleusCyclin-Dependent KinasesCyclinsEpitope MappingMaleMeiotic Prophase IMetaphaseMice, Inbred C57BLM Phase Cell Cycle CheckpointsMutationPachytene StageProliferating Cell Nuclear AntigenCNTD1 protein, mouseCyclin-Dependent KinasesCyclinsProliferating Cell Nuclear AntigenReplication Protein CRfc4 protein, mouseCDC34CDK1CDK2CNTD1meiosisMutLγrecombinationRFCubiquitylationWEE1

Identifiers

PMID32640224
PMCPMC7341696
OpenAlexW3041707238

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.