Evidence map›Paper›PMID 20733247›Full record

ArticlePhysical biology2010

The interplay of multiple feedback loops with post-translational kinetics results in bistability of mycobacterial stress response.

Abhinav Tiwari, Gábor Balázsi, Maria Laura Gennaro, Oleg A Igoshin

Open access · greenAbstract read
In one paragraph

Article in Physical biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
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

41 citing papers in PubMed, 75 citations in OpenAlex.

  1. PmrA Mutations in Drug-ResistantMicroorganisms · 2025
    Article
  2. Article
  3. Article
  4. Review
  5. Structure of the SigE regulatory network inFrontiers in microbiology · 2024
    Article
  6. Article
  7. Review
  8. SigE: A master regulator ofFrontiers in microbiology · 2023
    Review
  9. Article
  10. Article
  11. Review
  12. Transcriptional regulation and drug resistance inFrontiers in cellular and infection microbiology · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Towards multiscale modeling of the CD8Wiley interdisciplinary reviews. Systems biology and medicine · 2019
    Review
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

4 authors at 3 institutions in 1 country.

Abhinav TiwariDepartment of Bioengineering, Rice University, MS-142, 6100 Main St., Houston, TX 77005, USA.
Gábor Balázsi
Maria Laura Gennaro
Oleg A Igoshin
Rice University · USRutgers New Jersey Medical SchoolThe University of Texas MD Anderson Cancer Center · US

Funding

Mapping and modeling host-pathogen interactions in TB latency and reactivationR01HL106788 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI BALAZSI, GABOR, GENNARO, MARIA LAURA · 2010 to 2013
$3.1M
Connecting the selection of noisy gene expression deviants to genetic evolutionDP2OD006481 · OD · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BALAZSI, GABOR · 2009 to 2009
$2.3M
Feedback regulation and transcirptional coupling in bacterial stress-responseR01GM096189 · NIGMS · RICE UNIVERSITY · PI IGOSHIN, OLEG · 2010 to 2014
$1.3M
NIGMS NIH HHS GM096189-01NIGMS NIH HHS R01 GM096189NIH HHS DP2 OD006481
6 · The paper itself

Abstract

Bacterial persistence is the phenomenon in which a genetically identical fraction of a bacterial population can survive exposure to stress by reduction or cessation of growth. Persistence in mycobacteria has been recently linked to a stress-response network, consisting of the MprA/MprB two-component system and alternative sigma factor sigma(E). This network contains multiple positive transcriptional feedback loops which may give rise to bistability, making it a good candidate for controlling the mycobacterial persistence switch. To analyze the possibility of bistability, we develop a method that involves decoupling of the network into transcriptional and post-translational interaction modules. As a result we reduce the dimensionality of the dynamical system and independently analyze input-output relations in the two modules to formulate a necessary condition for bistability in terms of their logarithmic gains. We show that neither the positive autoregulation in the MprA/MprB network nor the sigma(E)-mediated transcriptional feedback is sufficient to induce bistability in a biochemically realistic parameter range. Nonetheless, inclusion of the post-translational regulation of sigma(E) by RseA increases the effective cooperativity of the system, resulting in bistability that is robust to parameter variation. We predict that overexpression or deletion of RseA, the key element controlling the ultrasensitive response, can eliminate bistability.

Indexed as

Feedback, PhysiologicalAlgorithmsBacterial ProteinsComputer SimulationKineticsMycobacterium tuberculosisProtein BiosynthesisSignal TransductionStress, PhysiologicalBacterial Proteins

Identifiers

PMID20733247
PMCPMC3543150
OpenAlexW2015523481

What OpenQuestion holds

Textmetadata
LicenceTDM
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.