Evidence map›Paper›PMID 31130236›Full record

ArticleBiophysical journal2019

The Effect of Tropomyosin Mutations on Actin-Tropomyosin Binding: In Search of Lost Time.

William Lehman, Jeffrey R Moore, Stuart G Campbell, Michael J Rynkiewicz

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 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.

William LehmanDepartment of Physiology and Biophysics, Boston University School of Medicine, Boston, Massachusetts. Electronic address: wlehman@bu.edu.
Jeffrey R MooreDepartment of Biological Sciences, University of Massachusetts-Lowell, Lowell, Massachusetts.
Stuart G CampbellDepartments of Biomedical Engineering and Cellular and Molecular Physiology, Yale University, New Haven, Connecticut.
Michael J RynkiewiczDepartment of Physiology and Biophysics, Boston University School of Medicine, Boston, Massachusetts.
Boston University · USUniversity of Massachusetts Lowell · USYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
THIN FILAMENTS AND VERTEBRATE SMOOTH MUSCLE CONTRACTIONR01HL036153 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI William J Lehman · 1986 to 2026
$6.5M
Revealing Pathomechanisms of Mutant TPM1 Through a Hybrid Computational-Experimental ApproachR01HL136590 · NHLBI · YALE UNIVERSITY · PI STUART G CAMPBELL, William J Lehman · 2017 to 2026
$5.6M
Cooperativity in the Cardiac Myofilament Interactome in Health and DiseaseR01HL123774 · NHLBI · UNIVERSITY OF MASSACHUSETTS LOWELL · PI MOORE, JEFFREY R · 2016 to 2019
$1.6M
NCATS NIH HHS UL1 TR001863NHLBI NIH HHS R01 HL036153NHLBI NIH HHS R01 HL123774NHLBI NIH HHS R01 HL136590
6 · The paper itself

Abstract

The initial binding of tropomyosin onto actin filaments and then its polymerization into continuous cables on the filament surface must be precisely tuned to overall thin-filament structure, function, and performance. Low-affinity interaction of tropomyosin with actin has to be sufficiently strong to localize the tropomyosin on actin, yet not so tight that regulatory movement on filaments is curtailed. Likewise, head-to-tail association of tropomyosin molecules must be favorable enough to promote tropomyosin cable formation but not so tenacious that polymerization precedes filament binding. Arguably, little molecular detail on early tropomyosin binding steps has been revealed since Wegner's seminal studies on filament assembly almost 40 years ago. Thus, interpretation of mutation-based actin-tropomyosin binding anomalies leading to cardiomyopathies cannot be described fully. In vitro, tropomyosin binding is masked by explosive tropomyosin polymerization once cable formation is initiated on actin filaments. In contrast, in silico analysis, characterizing molecular dynamics simulations of single wild-type and mutant tropomyosin molecules on F-actin, is not complicated by tropomyosin polymerization at all. In fact, molecular dynamics performed here demonstrates that a midpiece tropomyosin domain is essential for normal actin-tropomyosin interaction and that this interaction is strictly conserved in a number of tropomyosin mutant species. Elsewhere along these mutant molecules, twisting and bending corrupts the tropomyosin superhelices as they "lose their grip" on F-actin. We propose that residual interactions displayed by these mutant tropomyosin structures with actin mimic ones that occur in early stages of thin-filament generation, as if the mutants are recapitulating the assembly process but in reverse. We conclude therefore that an initial binding step in tropomyosin assembly onto actin involves interaction of the essential centrally located domain.

Indexed as

Molecular Dynamics SimulationMutationActinsAmino Acid SequenceProtein BindingProtein Structure, SecondaryTropomyosinActinsTropomyosin

Identifiers

PMID31130236
PMCPMC6588729
OpenAlexW2945399320

What OpenQuestion holds

Textmetadata
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.