Evidence map›Paper›PMID 25636358›Full record

ArticleNeural development2015

Polycomb group genes are required to maintain a binary fate choice in the Drosophila eye.

Jennifer K Finley, Adam C Miller, Tory G Herman

Open access · goldAbstract readComparative Study
In one paragraph

Article in Neural development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 43% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
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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

3 authors at 1 institution in 1 country.

Jennifer K FinleyInstitute of Molecular Biology, University of Oregon, 1370 Franklin Blvd, Eugene, OR, 97403, USA. Jennifer.Finley@ucsf.edu.
Adam C MillerInstitute of Molecular Biology, University of Oregon, 1370 Franklin Blvd, Eugene, OR, 97403, USA. amiller@fhcrc.org.
Tory G HermanInstitute of Molecular Biology, University of Oregon, 1370 Franklin Blvd, Eugene, OR, 97403, USA. herman@molbio.uoregon.edu.
University of Oregon · US

Funding

Graduate Training in Genetics Administrative Supplement - Career Curriculum DevelopmentT32GM007413 · NIGMS · UNIVERSITY OF OREGON · PI GUILLEMIN, KAREN J · 1985 to 2022
$7.8M
DEVELOPMENTAL BIOLOGY TRAINING PROGRAMT32HD007348 · NICHD · UNIVERSITY OF OREGON · PI Chris Q Doe, KRYN STANKUNAS · 1989 to 2026
$6.8M
NICHD NIH HHS T32 HD007348NIGMS NIH HHS 5-T32-GM007413NIGMS NIH HHS T32 GM007413
6 · The paper itself

Abstract

backgroundIdentifying the mechanisms by which cells remain irreversibly committed to their fates is a critical step toward understanding and being able to manipulate development and homeostasis. Polycomb group (PcG) proteins are chromatin modifiers that maintain transcriptional silencing, and loss of PcG genes causes widespread derepression of many developmentally important genes. However, because of their broad effects, the degree to which PcG proteins are used at specific fate choice points has not been tested. To understand how fate choices are maintained, we have been analyzing R7 photoreceptor neuron development in the fly eye. R1, R6, and R7 neurons are recruited from a pool of equivalent precursors. In order to adopt the R7 fate, these precursors make three binary choices. They: (1) adopt a neuronal fate, as a consequence of high receptor tyrosine kinase (RTK) activity (they would otherwise become non-neuronal support cells); (2) fail to express Seven-up (Svp), as a consequence of Notch (N) activation (they would otherwise express Svp and become R1/R6 neurons); and (3) fail to express Senseless (Sens), as a parallel consequence of N activation (they would otherwise express Sens and become R8 neurons in the absence of Svp). We were able to remove PcG genes specifically from post-mitotic R1/R6/R7 precursors, allowing us to probe these genes' roles in the three binary fate choices that R1/R6/R7 precursors face when differentiating as R7s.

resultsHere, we show that loss of the PcG genes Sce, Scm, or Pc specifically affects one of the three binary fate choices that R7 precursors must make: mutant R7s derepress Sens and adopt R8 fate characteristics. We find that this fate transformation occurs independently of the PcG genes' canonical role in repressing Hox genes. While N initially establishes Sens repression in R7s, we show that N is not required to keep Sens off, nor do these PcG genes act downstream of N. Instead, the PcG genes act independently of N to maintain Sens repression in R1/R6/R7 precursors that adopt the R7 fate.

conclusionsWe conclude that cells can use PcG genes specifically to maintain a subset of their binary fate choices.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsCell LineageChromatin Assembly and DisassemblyDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsGene Knockdown TechniquesGenes, HomeoboxGenes, InsectMutationNeurogenesisNuclear ProteinsPhenotypePhotoreceptor Cells, InvertebratePolycomb-Group ProteinsDNA-Binding ProteinsDrosophila ProteinsNuclear ProteinsPc protein, DrosophilaPolycomb-Group ProteinsPolycomb Repressive Complex 1Receptors, SteroidSce protein, DrosophilaSCM protein, Drosophilasens protein, Drosophilasvp protein, DrosophilaTranscription Factors

Identifiers

PMID25636358
PMCPMC4331296
OpenAlexW2138605160

What OpenQuestion 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 OpenQuestion graph.