Evidence map›Paper›PMID 31279009›Full record

ArticleThe Journal of allergy and clinical immunology2019

Mammalian diaphanous-related formin 1 (mDia1) coordinates mast cell migration and secretion through its actin-nucleating activity.

Ofir Klein, Rebecca A Krier-Burris, Pia Lazki-Hagenbach, Yaara Gorzalczany, Yang Mei, Peng Ji, Bruce S Bochner, Ronit Sagi-Eisenberg

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

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  12. Measurement of Exocytosis in Genetically Manipulated Mast Cells.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  13. 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

8 authors at 2 institutions in 2 countries.

Ofir KleinDepartment of Cell and Developmental Biology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Rebecca A Krier-BurrisDepartment of Medicine, Division of Allergy-Immunology, Northwestern University Feinberg School of Medicine, Chicago, Ill.
Pia Lazki-HagenbachDepartment of Cell and Developmental Biology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Yaara GorzalczanyDepartment of Cell and Developmental Biology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Yang MeiDepartment of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Ill.
Peng JiDepartment of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Ill.
Bruce S BochnerDepartment of Medicine, Division of Allergy-Immunology, Northwestern University Feinberg School of Medicine, Chicago, Ill.
Ronit Sagi-EisenbergDepartment of Cell and Developmental Biology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Electronic address: histol3@tauex.tau.ac.il.
Northwestern University · USTel Aviv University · IL

Funding

Using siglecs and their ligands to treat allergic diseases SALTADU19AI136443 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BOCHNER, BRUCE S · 2018 to 2022
$7.6M
Regulation of food allergy and anaphylaxis by IL 33R01AI105839 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BOCHNER, BRUCE S · 2014 to 2018
$1.8M
NIAID NIH HHS R01 AI105839NIAID NIH HHS U19 AI136443
6 · The paper itself

Abstract

backgroundActin remodeling is a key regulator of mast cell (MC) migration and secretion. However, the precise mechanism underlying the coordination of these processes has remained obscure.

objectiveWe sought to characterize the actin rearrangements that occur during MC secretion or chemotactic migration and identify the underlying mechanism of their coordination.

methodsUsing high-resolution microscopy, we analyzed the dynamics of actin rearrangements in MCs triggered to migration by IL-8 or prostaglandin E

resultsWe show that a major feature of the actin skeleton in MCs stimulated to migration is the buildup of pericentral actin clusters that prevent cell flattening and converge the secretory granules (SGs) in the cell center. This migratory phenotype is replaced on encounter of an IgE cross-linking antigen that stimulates secretion through a secretory phenotype characterized by cell flattening, reduction of actin mesh density, ruffling of cortical actin, and mobilization of SGs. Furthermore, we show that knockdown of mammalian diaphanous-related formin 1 (mDia1) inhibits chemotactic migration and its typical actin rearrangements, whereas expression of an active mDia1 mutant recapitulates the migratory actin phenotype and enhances cell migration while inhibiting FcεRI-triggered secretion. However, mice deficient in mDia1 appear to have normal numbers of MCs in various organs at baseline.

conclusionOur results demonstrate a unique role of actin rearrangements in clustering the SGs and inhibiting their secretion during MC migration. We identify mDia1 as a novel regulator of MC response that coordinates MC chemotaxis and secretion through its actin-nucleating activity.

Indexed as

Actin CytoskeletonAnimalsCell DegranulationCell MovementChemotaxis, LeukocyteForminsMast CellsMiceDiap1 protein, mouseForminsactinchemotaxisexocytosismammalian diaphanous-related formin 1Mast cells

Identifiers

PMID31279009
PMCPMC7278082
OpenAlexW2955960410

What OpenQuestion holds

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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.