Evidence map›Paper›PMID 33932332›Full record

ArticleDevelopmental cell2021

Toll receptors remodel epithelia by directing planar-polarized Src and PI3K activity.

Masako Tamada, Jay Shi, Kia S Bourdot, Sara Supriyatno, Karl H Palmquist, Omar L Gutierrez-Ruiz, Jennifer A Zallen

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 39 citations in OpenAlex.

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  17. A PtdIns(3,4,5)PDevelopmental cell · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Masako TamadaHoward Hughes Medical Institute and Developmental Biology Program, Sloan Kettering Institute, New York, NY, USA.
Jay ShiHoward Hughes Medical Institute and Developmental Biology Program, Sloan Kettering Institute, New York, NY, USA; Weill Cornell/Rockefeller/Sloan Kettering Tri-Institutional MD-PhD Program, New York, NY, USA.
Kia S BourdotHoward Hughes Medical Institute and Developmental Biology Program, Sloan Kettering Institute, New York, NY, USA.
Sara SupriyatnoHoward Hughes Medical Institute and Developmental Biology Program, Sloan Kettering Institute, New York, NY, USA.
Karl H PalmquistHoward Hughes Medical Institute and Developmental Biology Program, Sloan Kettering Institute, New York, NY, USA.
Omar L Gutierrez-RuizHoward Hughes Medical Institute and Developmental Biology Program, Sloan Kettering Institute, New York, NY, USA.
Jennifer A ZallenHoward Hughes Medical Institute and Developmental Biology Program, Sloan Kettering Institute, New York, NY, USA. Electronic address: zallenj@mskcc.org.
Howard Hughes Medical Institute · USCornell University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Molecular control of tissue morphogenesisR01GM079340 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI ZALLEN, JENNIFER A · 2007 to 2021
$4.2M
Dynamic Organization of Cell Architecture in Multicellular TissuesF30CA236441 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI SHI, JAY · 2019 to 2022
$183k
Howard Hughes Medical InstituteNCI NIH HHS F30 CA236441NCI NIH HHS P30 CA008748NIGMS NIH HHS R01 GM079340NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

Toll-like receptors are essential for animal development and survival, with conserved roles in innate immunity, tissue patterning, and cell behavior. The mechanisms by which Toll receptors signal to the nucleus are well characterized, but how Toll receptors generate rapid, localized signals at the cell membrane to produce acute changes in cell polarity and behavior is not known. We show that Drosophila Toll receptors direct epithelial convergent extension by inducing planar-polarized patterns of Src and PI3-kinase (PI3K) activity. Toll receptors target Src activity to specific sites at the membrane, and Src recruits PI3K to the Toll-2 complex through tyrosine phosphorylation of the Toll-2 cytoplasmic domain. Reducing Src or PI3K activity disrupts planar-polarized myosin assembly, cell intercalation, and convergent extension, whereas constitutive Src activity promotes ectopic PI3K and myosin cortical localization. These results demonstrate that Toll receptors direct cell polarity and behavior by locally mobilizing Src and PI3K activity.

Indexed as

ActomyosinAnimalsCell MembraneCell PolarityDrosophila melanogasterDrosophila ProteinsEmbryonic DevelopmentMorphogenesisPhosphatidylinositol 3-Kinasessrc-Family KinasesToll-Like ReceptorsActomyosinDrosophila ProteinsPhosphatidylinositol 3-Kinasessrc-Family KinasesToll-Like Receptorsactomyosin contractilityconvergent extensionDrosophilaepithelial morphogenesisPI3-kinaseplanar polaritySrcToll-like receptor

Identifiers

PMID33932332
PMCPMC8570296
OpenAlexW3159084180

What Socratic 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 Socratic graph.