Evidence map›Paper›PMID 35853502›Full record

ArticleDevelopmental biology2022

Lpt, trr, and Hcf regulate histone mono- and dimethylation that are essential for Drosophila heart development.

Wen Huang, Jun-Yi Zhu, Yulong Fu, Joyce van de Leemput, Zhe Han

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. International journal of molecular sciences · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. The Roles of Histone Lysine Methyltransferases in Heart Development and Disease.Journal of cardiovascular development and disease · 2023
    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

5 authors at 1 institution in 2 countries.

Wen HuangCenter for Precision Disease Modeling, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA; Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, Hunan, China.
Jun-Yi ZhuCenter for Precision Disease Modeling, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA; Division of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
Yulong FuCenter for Precision Disease Modeling, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA; Genomic Diagnostics and Bioinformatics, Department of Pathology, The University of Alabama at Birmingham, Alabama, USA.
Joyce van de LeemputCenter for Precision Disease Modeling, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA; Division of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
Zhe HanCenter for Precision Disease Modeling, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA; Division of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA. Electronic address: zhan@som.umaryland.edu.
University of Maryland, Baltimore · US

Funding

Modeling Nephrotic Syndrome in Drosophila NephrocytesR01DK098410 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI HAN, ZHE · 2014 to 2022
$3.3M
INCLUDE19-Ancestral roles of histone-modifying genes in heart development and diseaseR01HL134940 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI HAN, ZHE · 2017 to 2020
$2.4M
NHLBI NIH HHS R01 HL134940NIDDK NIH HHS R01 DK098410
6 · The paper itself

Abstract

Mammalian KMT2C, KMT2D, and HCFC1 are expressed during heart development and have been associated with congenital heart disease, but their roles in heart development remain elusive. We found that the Drosophila Lpt and trr genes encode the N-terminal and C-terminal homologs, respectively, of mammalian KMT2C or KMT2D. Lpt and trr mutant embryos showed reduced cardiac progenitor cells. Silencing of Lpt, trr, or both simultaneously in the heart led to similar abnormal cardiac morphology, tissue fibrosis, and cardiac functional defects. Like KMT2D, Lpt and trr were found to modulate histone H3K4 mono- and dimethylation, but not trimethylation. Investigation of downstream genes regulated by mouse KMT2D in the heart showed that their fly homologs are similarly regulated by Lpt or trr in the fly heart, suggesting that Lpt and trr regulate an evolutionarily conserved transcriptional network for heart development. Moreover, we showed that cardiac silencing of Hcf, the fly homolog of mammalian HCFC1, leads to heart defects similar to those observed in Lpt and trr silencing, as well as reduced H3K4 monomethylation. Our findings suggest that Lpt and trr function together to execute the conserved function of mammalian KMT2C and KMT2D in histone H3 lysine K4 mono- and dimethylation required for heart development. Possibly aided by Hcf, which we show plays a related role in H3K4 methylation during fly heart development.

Indexed as

Drosophila ProteinsHistone-Lysine N-MethyltransferaseHistonesNuclear Receptor CoactivatorsAnimalsDrosophilaMethylationMiceDrosophila ProteinsHistone-Lysine N-MethyltransferaseHistoneshost cell factor, DrosophilaLpt protein, DrosophilaNuclear Receptor CoactivatorsTRR protein, DrosophilaDrosophilaHcfHCFC1Heart developmentHistone modificationKMT2CKMT2DLptTrr

Identifiers

PMID35853502
PMCPMC10728806
OpenAlexW4285602917

What OpenQuestion holds

Textmetadata
LicenceTDM
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.