Evidence map›Paper›PMID 38960898›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society2024

Fibroblasts as an in vitro model of circadian genetic and genomic studies.

Marcelo Francia, Merel Bot, Toni Boltz, Juan F De la Hoz, Marco Boks, René S Kahn, Roel A Ophoff

Abstract read
In one paragraph

Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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  5. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Marcelo FranciaInterdepartmental Program for Neuroscience, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA. marcelofrancia@g.ucla.edu.
Merel BotCenter for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles, Los Angeles, CA, USA.
Toni BoltzDepartment of Human Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Juan F De la HozBioinformatics Interdepartamental Program, University of California Los Angeles, Los Angeles, CA, USA.
Marco BoksDepartment Psychiatry, Brain Center University Medical Center Utrecht, University Utrecht, Utrecht, The Netherlands.
René S KahnDepartment of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Roel A OphoffCenter for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles, Los Angeles, CA, USA.

Funding

Genomic Studies of Bipolar Disorder in a Large Cohort from The NetherlandsR01MH090553 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI OPHOFF, ROEL A · 2010 to 2014
$6.0M
Joint genomic and statistical analyses of schizophrenia and bipolar to decipher genetic susceptibilityR01MH115676 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Roel A Ophoff, Bogdan Pasaniuc · 2018 to 2026
$5.9M
Training Grant in Neurobehavioral GeneticsT32NS048004 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BEARDEN, CARRIE E, OPHOFF, ROEL A · 2004 to 2025
$5.8M
National Alliance for Research on Schizophrenia and Depression Distinguished Investigator GrantNIH HHS R01 MH090553NIMH NIH HHS R01 MH090553NIMH NIH HHS R01 MH115676NINDS NIH HHS T32 NS048004
6 · The paper itself

Abstract

Bipolar disorder (BD) is a heritable disorder characterized by shifts in mood that manifest in manic or depressive episodes. Clinical studies have identified abnormalities of the circadian system in BD patients as a hallmark of underlying pathophysiology. Fibroblasts are a well-established in vitro model for measuring circadian patterns. We set out to examine the underlying genetic architecture of circadian rhythm in fibroblasts, with the goal to assess its contribution to the polygenic nature of BD disease risk. We collected, from primary cell lines of 6 healthy individuals, temporal genomic features over a 48 h period from transcriptomic data (RNA-seq) and open chromatin data (ATAC-seq). The RNA-seq data showed that only a limited number of genes, primarily the known core clock genes such as ARNTL, CRY1, PER3, NR1D2 and TEF display circadian patterns of expression consistently across cell cultures. The ATAC-seq data identified that distinct transcription factor families, like those with the basic helix-loop-helix motif, were associated with regions that were increasing in accessibility over time. Whereas known glucocorticoid receptor target motifs were identified in those regions that were decreasing in accessibility. Further evaluation of these regions using stratified linkage disequilibrium score regression analysis failed to identify a significant presence of them in the known genetic architecture of BD, and other psychiatric disorders or neurobehavioral traits in which the circadian rhythm is affected. In this study, we characterize the biological pathways that are activated in this in vitro circadian model, evaluating the relevance of these processes in the context of the genetic architecture of BD and other disorders, highlighting its limitations and future applications for circadian genomic studies.

Indexed as

Bipolar DisorderCircadian RhythmFibroblastsChromatinGenomicsHumansTranscriptomeChromatin

Identifiers

PMID38960898
PMCPMC11329553

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Registered trials

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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.