Evidence map›Paper›PMID 37961332›Full record

ArticlebioRxiv : the preprint server for biology2023

Decoding Heterogenous Single-cell Perturbation Responses.

Bicna Song, Dingyu Liu, Weiwei Dai, Natalie McMyn, Qingyang Wang, Dapeng Yang, Adam Krejci, Anatoly Vasilyev, Nicole Untermoser, Anke Loregger and 14 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. 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

5 · Who and what money

Authors and funding

24 authors.

Bicna SongCenter for Genetic Medicine Research, Children's National Hospital, Washington DC, USA.
Dingyu LiuDevelopmental Biology Program, Sloan Kettering Institute, New York City, NY, USA.
Weiwei DaiDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Natalie McMynDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Qingyang WangDepartment of Statistics and Data Science, University of California, Los Angeles, CA, USA.
Dapeng YangDevelopmental Biology Program, Sloan Kettering Institute, New York City, NY, USA.
Adam KrejciMyllia Biotechnology GmbH. Am Kanal 27, 1110 Vienna Austria.
Anatoly VasilyevMyllia Biotechnology GmbH. Am Kanal 27, 1110 Vienna Austria.
Nicole UntermoserMyllia Biotechnology GmbH. Am Kanal 27, 1110 Vienna Austria.
Anke LoreggerMyllia Biotechnology GmbH. Am Kanal 27, 1110 Vienna Austria.
Dongyuan SongBioinformatics Interdepartmental Ph.D. Program, University of California, Los Angeles, CA, USA.
Breanna WilliamsDevelopmental Biology Program, Sloan Kettering Institute, New York City, NY, USA.
Bess RosenDevelopmental Biology Program, Sloan Kettering Institute, New York City, NY, USA.
Xiaolong ChengCenter for Genetic Medicine Research, Children's National Hospital, Washington DC, USA.
Lumen ChaoCenter for Genetic Medicine Research, Children's National Hospital, Washington DC, USA.
Hanuman T KaleDevelopmental Biology Program, Sloan Kettering Institute, New York City, NY, USA.
Hao ZhangDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Yarui DiaoDepartment of Cell Biology, Duke University Medical Center, Durham, NC, USA.
Tilmann BürckstümmerMyllia Biotechnology GmbH. Am Kanal 27, 1110 Vienna Austria.
Jenet M SilicianoDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Jingyi Jessica LiDepartment of Statistics and Data Science, University of California, Los Angeles, CA, USA.
Robert SilicianoDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Danwei HuangfuDevelopmental Biology Program, Sloan Kettering Institute, New York City, NY, USA.
Wei LiCenter for Genetic Medicine Research, Children's National Hospital, Washington DC, USA.ORCID 0000-0002-2163-7903

Funding

SWG 2: Cure Research Scientific Working GroupP30AI117970 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI Italo Mocchetti · 2015 to 2026
$29.6M
Center for scalable knockout and multimodal phenotyping in genetically diverse human genomesUM1HG012654 · NHGRI · SLOAN-KETTERING INST CAN RESEARCH · PI Danwei Huangfu, LORENZ P. STUDER · 2022 to 2026
$9.1M
Genomic control of gene regulatory networks governing early human lineagedecisionsU01HG012051 · NHGRI · SLOAN-KETTERING INST CAN RESEARCH · PI Michael A Beer, ANNA-KATERINA HADJANTONAKIS · 2021 to 2026
$8.3M
Integrative genomic and functional genomic studies to connect variant to function for CAD GWAS lociR01HL168174 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Wei Li, EDOARDO MARCORA · 2023 to 2026
$3.1M
Modeling Heterogenous Outcomes in Functional Genetic Screens Using Single-cell Genomics as ReadoutsR01HG010753 · NHGRI · CHILDREN'S RESEARCH INSTITUTE · PI LI, WEI · 2019 to 2023
$2.5M
Statistical Methods for Elucidating Regulatory Mechanisms and Functional Impacts of Transcriptome Variation at Population and Single-Cell ScalesR35GM140888 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LI, JINGYI JESSICA · 2021 to 2025
$2.0M
NHGRI NIH HHS R01 HG010753NHGRI NIH HHS U01 HG012051NHGRI NIH HHS UM1 HG012654NHLBI NIH HHS R01 HL168174NIAID NIH HHS P30 AI117970NIGMS NIH HHS R35 GM140888
6 · The paper itself

Abstract

Understanding diverse responses of individual cells to the same perturbation is central to many biological and biomedical problems. Current methods, however, do not precisely quantify the strength of perturbation responses and, more importantly, reveal new biological insights from heterogeneity in responses. Here we introduce the perturbation-response score (PS), based on constrained quadratic optimization, to quantify diverse perturbation responses at a single-cell level. Applied to single-cell transcriptomes of large-scale genetic perturbation datasets (e.g., Perturb-seq), PS outperforms existing methods for quantifying partial gene perturbation responses. In addition, PS presents two major advances. First, PS enables large-scale, single-cell-resolution dosage analysis of perturbation, without the need to titrate perturbation strength. By analyzing the dose-response patterns of over 2,000 essential genes in Perturb-seq, we identify two distinct patterns, depending on whether a moderate reduction in their expression induces strong downstream expression alterations. Second, PS identifies intrinsic and extrinsic biological determinants of perturbation responses. We demonstrate the application of PS in contexts such as T cell stimulation, latent HIV-1 expression, and pancreatic cell differentiation. Notably, PS unveiled a previously unrecognized, cell-type-specific role of coiled-coil domain containing 6 (CCDC6) in guiding liver and pancreatic lineage decisions, where CCDC6 knockouts drive the endoderm cell differentiation towards liver lineage, rather than pancreatic lineage. The PS approach provides an innovative method for dose-to-function analysis and will enable new biological discoveries from single-cell perturbation datasets.

Indexed as

computational modelCRISPR-based genetic perturbationsPerturb-seqsingle-cell RNA-seq

Identifiers

PMID37961332
PMCPMC10635009

What OpenQuestion holds

Textmetadata
LicenceCC BY-ND
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.