Evidence map›Paper›PMID 33604655›Full record

ArticleThe Journal of cell biology2021

SUV39H2 epigenetic silencing controls fate conversion of epidermal stem and progenitor cells.

Pierre Balmer, William V J Hariton, Beyza S Sayar, Vidhya Jagannathan, Arnaud Galichet, Tosso Leeb, Petra Roosje, Eliane J Müller

Open access · greenAbstract read
In one paragraph

Article in The Journal of cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Pierre BalmerDivision of Clinical Dermatology, Department of Clinical Veterinary Medicine, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
William V J HaritonDermfocus, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
Beyza S SayarDermfocus, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
Vidhya JagannathanDermfocus, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
Arnaud GalichetDermfocus, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
Tosso LeebDermfocus, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
Petra Roosje *Division of Clinical Dermatology, Department of Clinical Veterinary Medicine, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
Eliane J Müller *Dermfocus, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
University of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic histone trimethylation on lysine 9 (H3K9me3) represents a major molecular signal for genome stability and gene silencing conserved from worms to man. However, the functional role of the H3K9 trimethylases SUV39H1/2 in mammalian tissue homeostasis remains largely unknown. Here, we use a spontaneous dog model with monogenic inheritance of a recessive SUV39H2 loss-of-function variant and impaired differentiation in the epidermis, a self-renewing tissue fueled by stem and progenitor cell proliferation and differentiation. Our results demonstrate that SUV39H2 maintains the stem and progenitor cell pool by restricting fate conversion through H3K9me3 repressive marks on gene promoters encoding components of the Wnt/p63/adhesion axis. When SUV39H2 function is lost, repression is relieved, and enhanced Wnt activity causes progenitor cells to prematurely exit the cell cycle, a process mimicked by pharmacological Wnt activation in primary canine, human, and mouse keratinocytes. As a consequence, the stem cell growth potential of cultured SUV39H2-deficient canine keratinocytes is exhausted while epidermal differentiation and genome stability are compromised. Collectively, our data identify SUV39H2 and potentially also SUV39H1 as major gatekeepers in the delicate balance of progenitor fate conversion through H3K9me3 rate-limiting road blocks in basal layer keratinocytes.

Indexed as

Cell DifferentiationCell ProliferationGene Expression Regulation, EnzymologicGene SilencingWnt Signaling PathwayAnimalsDogsEpidermisFemaleHistone-Lysine N-MethyltransferaseHumansKeratinocytesLoss of Function MutationMaleMiceStem CellsHistone-Lysine N-Methyltransferase

Identifiers

PMID33604655
PMCPMC7898489
OpenAlexW3132377632

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.