Evidence map›Paper›PMID 22829755›Full record

ArticlePLoS computational biology2012

Modular design of artificial tissue homeostasis: robust control through synthetic cellular heterogeneity.

Miles Miller, Marc Hafner, Eduardo Sontag, Noah Davidsohn, Sairam Subramanian, Priscilla E M Purnick, Douglas Lauffenburger, Ron Weiss

Abstract read
In one paragraph

Article in PLoS computational biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. An Artificial Tissue Homeostasis Circuit Designed via Analog Circuit Techniques.IEEE transactions on biomedical circuits and systems · 2019
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Fundamental trade-offs between information flow in single cells and cellular populations.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  10. Review
  11. Synthetic Morphogenesis.Cold Spring Harbor perspectives in biology · 2016
    Review
  12. Control theory meets synthetic biology.Journal of the Royal Society, Interface · 2016
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Modular composition of gene transcription networks.PLoS computational biology · 2014
    Article
  18. Logarithmic Lipschitz norms and diffusion-induced instability.Nonlinear analysis, theory, methods & applications · 2013
    Article
  19. Review
  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

8 authors.

Miles MillerDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America.
Marc Hafner
Eduardo Sontag
Noah Davidsohn
Sairam Subramanian
Priscilla E M Purnick
Douglas Lauffenburger
Ron Weiss

Funding

Collaborative Research: Multistability in Biological NetworksR01GM086881 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI CRACIUN, GHEORGHE · 2008 to 2012
$1.5M
NIGMS NIH HHS R01 GM086881NIGMS NIH HHS R01GM086881
6 · The paper itself

Abstract

Synthetic biology efforts have largely focused on small engineered gene networks, yet understanding how to integrate multiple synthetic modules and interface them with endogenous pathways remains a challenge. Here we present the design, system integration, and analysis of several large scale synthetic gene circuits for artificial tissue homeostasis. Diabetes therapy represents a possible application for engineered homeostasis, where genetically programmed stem cells maintain a steady population of β-cells despite continuous turnover. We develop a new iterative process that incorporates modular design principles with hierarchical performance optimization targeted for environments with uncertainty and incomplete information. We employ theoretical analysis and computational simulations of multicellular reaction/diffusion models to design and understand system behavior, and find that certain features often associated with robustness (e.g., multicellular synchronization and noise attenuation) are actually detrimental for tissue homeostasis. We overcome these problems by engineering a new class of genetic modules for 'synthetic cellular heterogeneity' that function to generate beneficial population diversity. We design two such modules (an asynchronous genetic oscillator and a signaling throttle mechanism), demonstrate their capacity for enhancing robust control, and provide guidance for experimental implementation with various computational techniques. We found that designing modules for synthetic heterogeneity can be complex, and in general requires a framework for non-linear and multifactorial analysis. Consequently, we adapt a 'phenotypic sensitivity analysis' method to determine how functional module behaviors combine to achieve optimal system performance. We ultimately combine this analysis with Bayesian network inference to extract critical, causal relationships between a module's biochemical rate-constants, its high level functional behavior in isolation, and its impact on overall system performance once integrated.

Indexed as

Models, BiologicalBayes TheoremCell Physiological PhenomenaComputer SimulationGene Regulatory NetworksHEK293 CellsHomeostasisHumansInsulin-Secreting CellsPhenotypeStem CellsSynthetic BiologySystems Biology

Identifiers

PMID22829755
PMCPMC3400602

What OpenQuestion holds

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LicenceCC BY
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.