Evidence map›Paper›PMID 38991050›Full record

ArticlePLoS computational biology2024

Role of diffusion and reaction of the constituents in spreading of histone modification marks.

Vinoth Manivannan, Mandar M Inamdar, Ranjith Padinhateeri

Abstract read
In one paragraph

Article in PLoS computational 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
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1 · What the graph read from it

What it found

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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

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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

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

3 authors.

Vinoth ManivannanDepartment of Biosciences and Bioengineering, Indian Institute of Technology Bombay, Mumbai, India.
Mandar M InamdarDepartment of Civil Engineering, Indian Institute of Technology Bombay, Mumbai, India.
Ranjith PadinhateeriDepartment of Biosciences and Bioengineering, Indian Institute of Technology Bombay, Mumbai, India.ORCID 0000-0001-5485-1474

Funding

Science and Engineering Research Board (SERB) CRG/2022/007974Sunita Sanghi Centre of Aging and Neurodegenerative Diseases (SCAN)
6 · The paper itself

Abstract

Cells switch genes ON or OFF by altering the state of chromatin via histone modifications at specific regulatory locations along the chromatin polymer. These gene regulation processes are carried out by a network of reactions in which the histone marks spread to neighboring regions with the help of enzymes. In the literature, this spreading has been studied as a purely kinetic, non-diffusive process considering the interactions between neighboring nucleosomes. In this work, we go beyond this framework and study the spreading of modifications using a reaction-diffusion (RD) model accounting for the diffusion of the constituents. We quantitatively segregate the modification profiles generated from kinetic and RD models. The diffusion and degradation of enzymes set a natural length scale for limiting the domain size of modification spreading, and the resulting enzyme limitation is inherent in our model. We also demonstrate the emergence of confined modification domains without the explicit requirement of a nucleation site. We explore polymer compaction effects on spreading and show that single-cell domains may differ from averaged profiles. We find that the modification profiles from our model are comparable with existing H3K9me3 data of S. pombe.

Indexed as

HistonesChromatinComputational BiologyDiffusionHistone CodeKineticsNucleosomesProtein Processing, Post-TranslationalSchizosaccharomycesChromatinHistonesNucleosomes

Identifiers

PMID38991050
PMCPMC11265668

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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.