Evidence map›Paper›PMID 21200415›Full record

ArticlePLoS computational biology2010

Kinetics of rhodopsin deactivation and its role in regulating recovery and reproducibility of rod photoresponse.

Giovanni Caruso, Paolo Bisegna, Leonardo Lenoci, Daniele Andreucci, Vsevolod V Gurevich, Heidi E Hamm, Emmanuele DiBenedetto

Abstract read
In one paragraph

Article in PLoS computational biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The phototransduction machinery in the rod outer segment has a strong efficacy gradient.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. The functional cycle of visual arrestins in photoreceptor cells.Progress in retinal and eye research · 2011
    Review
  17. Identification of key factors that reduce the variability of the single photon response.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  18. Article
  19. 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

7 authors.

Giovanni CarusoConstruction Technologies Institute, National Research Council, Rome, Italy.
Paolo Bisegna
Leonardo Lenoci
Daniele Andreucci
Vsevolod V Gurevich
Heidi E Hamm
Emmanuele DiBenedetto

Funding

STRUCTURE/FUNCTION STUDIES OF VISUAL ARRESTINR01EY011500 · NEI · VANDERBILT UNIVERSITY · PI T M Iverson · 1997 to 2026
$12.3M
IMMUNOLOGICAL STUDIES OF VISUAL TRANSDUCTION PATHWAYSR01EY006062 · NEI · VANDERBILT UNIVERSITY · PI HAMM, HEIDI E · 1985 to 2017
$5.6M
Mathematical Models of Dynamics of Visual TransductionR01GM068953 · NIGMS · VANDERBILT UNIVERSITY · PI DIBENEDETTO, EMMANUELE · 2003 to 2006
$933k
NEI NIH HHS EY006062NEI NIH HHS EY011500NEI NIH HHS R01 EY006062NEI NIH HHS R01 EY011500NIGMS NIH HHS 1R01GM068953NIGMS NIH HHS R01 GM068953
6 · The paper itself

Abstract

The single photon response (SPR) in vertebrate phototransduction is regulated by the dynamics of R* during its lifetime, including the random number of phosphorylations, the catalytic activity and the random sojourn time at each phosphorylation level. Because of this randomness the electrical responses are expected to be inherently variable. However the SPR is highly reproducible. The mechanisms that confer to the SPR such a low variability are not completely understood. The kinetics of rhodopsin deactivation is investigated by a Continuous Time Markov Chain (CTMC) based on the biochemistry of rhodopsin activation and deactivation, interfaced with a spatio-temporal model of phototransduction. The model parameters are extracted from the photoresponse data of both wild type and mutant mice, having variable numbers of phosphorylation sites and, with the same set of parameters, the model reproduces both WT and mutant responses. The sources of variability are dissected into its components, by asking whether a random number of turnoff steps, a random sojourn time between steps, or both, give rise to the known variability. The model shows that only the randomness of the sojourn times in each of the phosphorylated states contributes to the Coefficient of Variation (CV) of the response, whereas the randomness of the number of R* turnoff steps has a negligible effect. These results counter the view that the larger the number of decay steps of R*, the more stable the photoresponse is. Our results indicate that R* shutoff is responsible for the variability of the photoresponse, while the diffusion of the second messengers acts as a variability suppressor.

Indexed as

Models, NeurologicalRhodopsinAnimalsArrestinComputational BiologyG-Protein-Coupled Receptor Kinase 1KineticsMarkov ChainsMiceMice, TransgenicPhosphorylationPhotonsReproducibility of ResultsRetinal Rod Photoreceptor CellsArrestinG-Protein-Coupled Receptor Kinase 1Rhodopsin

Identifiers

PMID21200415
PMCPMC3002991

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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 OpenQuestion graph.