Evidence mapPaperPMID 37800333Full record

ArticleDevelopment (Cambridge, England)2023

KDM5-mediated activation of genes required for mitochondrial biology is necessary for viability in Drosophila.

Michael F Rogers, Owen J Marshall, Julie Secombe

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2023. 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
1.2field-weighted citation impact, top 20% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
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

3 authors at 2 institutions in 2 countries.

Michael F RogersDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.ORCID 0000-0002-6570-5031
Owen J MarshallMenzies Institute for Medical Research, University of Tasmania, Hobart TAS 7000, Australia.ORCID 0000-0003-1605-3871
Julie SecombeDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.ORCID 0000-0002-5826-7547
Albert Einstein College of Medicine · USUniversity of Tasmania · AU

Funding

WORD PROCESSORP30CA013330 · YESHIVA UNIVERSITY · 1985 to 2025
$27.5M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · YESHIVA UNIVERSITY · 1985 to 2005
$8.4M
Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · TRUSTEES OF INDIANA UNIVERSITY · 2025 to 2025
$1.7M
Distinct modes of gene expression by KDM5R01GM112783 · NIGMS · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI Julie Secombe · 2022 to 2022
$336k
NCI NIH HHS P30 CA013330NIGMS NIH HHS R01 GM112783NIGMS NIH HHS T32 GM007288NIH HHS P40 OD018537NIH HHS R01GM112783NIH HHS T32GM007288
6 · The paper itself

Abstract

Histone-modifying proteins play important roles in the precise regulation of the transcriptional programs that coordinate development. KDM5 family proteins interact with chromatin through demethylation of H3K4me3 as well as demethylase-independent mechanisms that remain less understood. To gain fundamental insights into the transcriptional activities of KDM5 proteins, we examined the essential roles of the single Drosophila Kdm5 ortholog during development. KDM5 performs crucial functions in the larval neuroendocrine prothoracic gland, providing a model to study its role in regulating key gene expression programs. Integrating genome binding and transcriptomic data, we identify that KDM5 regulates the expression of genes required for the function and maintenance of mitochondria, and we find that loss of KDM5 causes morphological changes to mitochondria. This is key to the developmental functions of KDM5, as expression of the mitochondrial biogenesis transcription factor Ets97D, homolog of GABPα, is able to suppress the altered mitochondrial morphology as well as the lethality of Kdm5 null animals. Together, these data establish KDM5-mediated cellular functions that are important for normal development and could contribute to KDM5-linked disorders when dysregulated.

Indexed as

DrosophilaDrosophila ProteinsAnimalsBiologyChromatinHistone DemethylasesChromatinDrosophila ProteinsHistone DemethylasesDemethylaseKDM5MitochondriaProthoracic glandTranscription

Identifiers

PMID37800333
PMCPMC10651110
OpenAlexW4387392261

What Socratic holds

Textmetadata
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 Socratic graph.