Evidence map›Paper›PMID 41968902›Full record

ArticleDevelopment (Cambridge, England)2026

PTEN regulates starburst amacrine cell dendrite morphology during development.

Teva W Bracha, Nina Luong, Joseph Leffler, Benjamin Sivyer, Kevin M Wright

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Teva W BrachaNeuroscience Graduate Program, Oregon Health & Science University, Portland, OR 97239, USA.
Nina LuongNeuroscience Graduate Program, Oregon Health & Science University, Portland, OR 97239, USA.
Joseph LefflerCasey Eye Institute, Oregon Health & Science University, Portland, OR 97239, USA.
Benjamin SivyerCasey Eye Institute, Oregon Health & Science University, Portland, OR 97239, USA.
Kevin M WrightVollum Institute, Oregon Health & Science University, Portland, OR 97239, USA.ORCID 0000-0001-5094-5270

Funding

Travel Grant PA-18-591T32NS007466 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI Kelly R Monk, Kevin Wright · 1999 to 2026
$7.0M
Translational Vision Science Research at Oregon Health & Science UniversityT32EY023211 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Yali Jia, Kate E Keller · 2013 to 2026
$2.4M
Functional subtypes of retinal ganglion cell photoreceptorsR01EY032564 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Joseph Leffler · 2022 to 2026
$2.2M
Transcriptional control of retinal neuron specification and maturation.R01EY032057 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI WRIGHT, KEVIN · 2021 to 2025
$2.1M
NEI NIH HHS R01EY032057NEI NIH HHS R01EY032564NEI NIH HHS T32EY023211NEI NIH HHS T32NS007466NINDS NIH HHSNINDS NIH HHS T32NS007466
6 · The paper itself

Abstract

Neurons are subject to extensive developmental regulation to ensure precise subtype-specific morphologies that are intimately tied to their function. Starburst amacrine cells (SACs) in the mammalian retina have a highly stereotyped, radially symmetric dendritic arbor that is essential for their role in direction-selective circuits in the retina. We show that PTEN, the primary negative regulator of the PI3K-AKT-mTOR pathway that is highly implicated in neurodevelopmental disorders, regulates SAC morphology in a cell-autonomous manner. Pten-deficient mouse SACs show a nearly twofold increase in the number of dendritic branches, while other morphological properties remain largely unchanged. These morphological changes arise late in SAC development, after dendrite development is largely complete, and persist into adulthood. Mechanistically, excessive dendritic branching appears to arise from dysregulated mTOR activity. Despite this increase in dendritic branches, Pten-deficient SACs maintain a normal population number, normal organization of synaptic outputs and intact direction-selectivity in the retina. Collectively, these results show that PTEN is essential in mouse for the normal development of highly stereotyped neuronal morphology.

Indexed as

Amacrine CellsDendritesPTEN PhosphohydrolaseAnimalsMiceMice, KnockoutNeurodevelopmentRetinaSignal TransductionTOR Serine-Threonine KinasesmTOR protein, mousePTEN PhosphohydrolasePten protein, mouseTOR Serine-Threonine KinasesDendriteMorphologyNeuronPTENRetina

Identifiers

PMID41968902
PMCPMC13200731

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Registered trials

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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.