Evidence map›Paper›PMID 38352569›Full record

ArticlebioRxiv : the preprint server for biology2024

Deciphering regulatory architectures from synthetic single-cell expression patterns.

Rosalind Wenshan Pan, Tom Röschinger, Kian Faizi, Hernan Garcia, Rob Phillips

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. 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

5 authors.

Rosalind Wenshan PanDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA.ORCID 0009-0005-0778-3794
Tom RöschingerDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA.ORCID 0000-0002-4900-3216
Kian FaiziDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA.ORCID 0000-0003-1306-0320
Hernan GarciaBiophysics Graduate Group, University of California, Berkeley, CA.ORCID 0000-0002-5212-3649
Rob PhillipsDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA.ORCID 0000-0003-3082-2809

Funding

The Principles of Regulatory, Conformational and Evolutionary AdaptationR35GM118043 · NIGMS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI ROB PHILLIPS · 2016 to 2026
$7.9M
NIGMS NIH HHS R35 GM118043
6 · The paper itself

Abstract

For the vast majority of genes in sequenced genomes, there is limited understanding of how they are regulated. Without such knowledge, it is not possible to perform a quantitative theory-experiment dialogue on how such genes give rise to physiological and evolutionary adaptation. One category of high-throughput experiments used to understand the sequence-phenotype relationship of the transcriptome is massively parallel reporter assays (MPRAs). However, to improve the versatility and scalability of MPRA pipelines, we need a "theory of the experiment" to help us better understand the impact of various biological and experimental parameters on the interpretation of experimental data. These parameters include binding site copy number, where a large number of specific binding sites may titrate away transcription factors, as well as the presence of overlapping binding sites, which may affect analysis of the degree of mutual dependence between mutations in the regulatory region and expression levels. To that end, in this paper we create tens of thousands of synthetic single-cell gene expression outputs using both equilibrium and out-of-equilibrium models. These models make it possible to imitate the summary statistics (information footprints and expression shift matrices) used to characterize the output of MPRAs and from this summary statistic to infer the underlying regulatory architecture. Specifically, we use a more refined implementation of the so-called thermodynamic models in which the binding energies of each sequence variant are derived from energy matrices. Our simulations reveal important effects of the parameters on MPRA data and we demonstrate our ability to optimize MPRA experimental designs with the goal of generating thermodynamic models of the transcriptome with base-pair specificity. Further, this approach makes it possible to carefully examine the mapping between mutations in binding sites and their corresponding expression profiles, a tool useful not only for better designing MPRAs, but also for exploring regulatory evolution.

Identifiers

PMID38352569
PMCPMC10862715

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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.