Evidence map›Paper›PMID 15758173›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

A differentially autoregulated Pet-1 enhancer region is a critical target of the transcriptional cascade that governs serotonin neuron development.

Michael M Scott, Katherine C Krueger, Evan S Deneris

Abstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed.

  1. Article
  2. A discrete serotonergic circuit involved in the generation of tinnitus behavior.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. iScience · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. p38α MAPK signaling drives pharmacologically reversible brain and gastrointestinal phenotypes in the SERT Ala56 mouse.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  8. Serotonin neuron development: shaping molecular and structural identities.Wiley interdisciplinary reviews. Developmental biology · 2018
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Gαi/o-coupled receptor signaling restricts pancreatic β-cell expansion.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  15. Article
  16. Article
  17. Review
  18. Subset specification of central serotonergic neurons.Frontiers in cellular neuroscience · 2013
    Review
  19. Transposon-mediated transgenesis, transgenic rescue, and tissue-specific gene expression in rodents and rabbits.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    Article
  20. 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.

Michael M ScottDepartment of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA.
Katherine C Krueger
Evan S Deneris

Funding

PET 1 ETS FACTOR IN THE MAMMALIAN 5 HT SYSTEMR01MH062723 · NIMH · CASE WESTERN RESERVE UNIVERSITY · PI DENERIS, EVAN S · 2001 to 2021
$8.3M
NIMH NIH HHS MH62723NIMH NIH HHS R01 MH062723
6 · The paper itself

Abstract

The Pet-1 [pheochromocytoma 12 ETS (E26 transformation-specific)] gene plays a critical role in the development of serotonin (5-HT)-modulated behaviors via its control of embryonic 5-HT neuron differentiation. Pet-1 transcription is induced exclusively in 5-HT neuron postmitotic precursors before the appearance of transmitter, and its restricted expression is maintained in the adult. However, the mechanisms that direct Pet-1 expression to this single CNS neuronal cell type are unknown. Here, we show, using transgenic methods, that genomic sequences upstream, but not downstream or within the Pet-1-coding region, are sufficient for 5-HT neuron-specific transgene expression. Enhancer sequences within a 40 kb upstream fragment directed position-independent lacZ (beta-D-galactosidase) transgene expression to the developing hindbrain before the appearance of 5-HT. Moreover, virtually all of the 5-HT neurons in the adult were lacZ positive in all of the lines examined. Transgene expression in 5-HT neurons was maintained when the 40 kb fragment was truncated on its 5' end to either 12 or 1.8 kb, although position independence was then lost. Analysis of transgene expression in Pet-1 null mice indicated that Pet-1 was required to maintain the activity of the Pet-1 enhancer region in a subset of 5-HT neurons. These findings suggest that a conserved 1.8 kb region immediately flanking the Pet-1-coding region is a critical genomic target of the transcriptional cascade that governs 5-HT neuron development and provide additional evidence for 5-HT neuron heterogeneity at the genetic level. We discuss the potential application of the Pet-1 transgenes reported here to the selective genetic manipulation of 5-HT neurons.

Indexed as

AnimalsCell DifferentiationEnhancer Elements, GeneticHomeostasisHumansMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeuronsSerotoninTranscriptional ActivationTranscription FactorsTransgenesFev protein, ratSerotoninTranscription Factors

Identifiers

PMID15758173
PMCPMC6725185

What OpenQuestion holds

Textmetadata
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.