Evidence map›Paper›PMID 40027702›Full record

ArticlebioRxiv : the preprint server for biology2025

CellPHIE: Integrating Pathway Discovery With Pooled Profiling of Perturbations Uncovers Pathways of Huntington's Disease, Including Genetic Modifiers of Neuronal Development and Morphology.

Byunguk Kang, Michael Murphy, Christopher W Ng, Matthew Joseph Leventhal, Nhan Huynh, Egun Im, Serwah Danquah, David E Housman, Ralda Nehme, Samouil L Farhi and 1 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Byunguk KangDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID 0009-0004-5540-7745
Michael MurphyDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Christopher W NgDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.
Matthew Joseph LeventhalDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Nhan HuynhDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Egun ImDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Serwah DanquahSpatial Technology Platform, Broad Institute of Harvard and MIT, Cambridge, MA USA.
David E HousmanDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.
Ralda NehmeStanley Center for Psychiatric Research, Broad Institute of Harvard and MIT, Cambridge, MA, USA.ORCID 0000-0001-7215-3311
Samouil L FarhiSpatial Technology Platform, Broad Institute of Harvard and MIT, Cambridge, MA USA.ORCID 0000-0003-1359-4568
Ernest FraenkelDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID 0000-0001-9249-8181

Funding

Epigenetic Pathology and Therapy in Huntington's DiseaseR01NS089076 · NINDS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI FRAENKEL, ERNEST, HOUSMAN, DAVID · 2015 to 2024
$4.9M
Graduate Training in Computational and Systems BiologyT32GM087237 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BURGE, CHRISTOPHER B · 2009 to 2023
$4.6M
Unraveling the Genetic Programs Engaged in ASD Neurons Through Coupled Transcriptomic and Phenotypic ReadoutsR01MH128366 · NIMH · BROAD INSTITUTE, INC. · PI Samouil Farhi, Ralda Nehme · 2022 to 2026
$3.7M
NIGMS NIH HHS T32 GM087237NIMH NIH HHS R01 MH128366NINDS NIH HHS R01 NS089076
6 · The paper itself

Abstract

Genomic screens and GWAS are powerful tools for identifying disease-modifying genes, but it is often challenging to understand the pathways by which these genes function. Here, we take an integrated approach that combines network analysis and an imaging-based pooled genetic perturbation study to examine modifiers of Huntington's disease (HD). The computational analysis highlighted several genes in a subnetwork enriched for modifiers of neuronal development and morphology. To test the functional roles of these genes, we developed an experimental pipeline that allows pooled CRISPRi KD of 21 genes in human iPSC-derived neurons followed by optical analysis of genotypes, neuronal arborization, multiplexed pathway activity and morphological fingerprint readout. This approach recovered known genes involved in morphology and confirmed unexpected links from the network between several genetic modifiers of HD and morphology. Our approach overcomes challenges in pooled measurement of neuronal function and health and could be adapted for other phenotypes in HD and other neurological diseases.

Identifiers

PMID40027702
PMCPMC11870572

What Socratic holds

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LicenceCC BY-NC
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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 Socratic graph.