Evidence map›Paper›PMID 26824654›Full record

ArticleCell2016

Toll Receptor-Mediated Hippo Signaling Controls Innate Immunity in Drosophila.

Bo Liu, Yonggang Zheng, Feng Yin, Jianzhong Yu, Neal Silverman, Duojia Pan

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed, 1 pooled it
18.2field-weighted citation impact, top 1% 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

140 citing papers in PubMed, 1 synthesis or guideline pooled it, 253 citations in OpenAlex.

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80 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Bo LiuDepartment of Molecular Biology and Genetics, Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Yonggang ZhengDepartment of Molecular Biology and Genetics, Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Feng YinDepartment of Molecular Biology and Genetics, Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Jianzhong YuDepartment of Molecular Biology and Genetics, Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Neal SilvermanDivision of Infectious Diseases, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Duojia PanDepartment of Molecular Biology and Genetics, Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address: djpan@jhmi.edu.
Howard Hughes Medical Institute · USUniversity of Massachusetts Chan Medical School · US

Funding

From Drosophila Immunity to Anti-InflammatoriesR01AI060025 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Neal Silverman · 2004 to 2026
$9.4M
Control of Cell Number in Developing RetinaR01EY015708 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI DUOJIA PAN · 2004 to 2026
$8.8M
Activation of Insect Immunity by Gram-Negative BacteriaR56AI060025 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SILVERMAN, NEAL · 2011 to 2017
$459k
Howard Hughes Medical InstituteNEI NIH HHS EY015708NEI NIH HHS R01 EY015708NIAID NIH HHS AI060025NIAID NIH HHS R01 AI060025
6 · The paper itself

Abstract

The Hippo signaling pathway functions through Yorkie to control tissue growth and homeostasis. How this pathway regulates non-developmental processes remains largely unexplored. Here, we report an essential role for Hippo signaling in innate immunity whereby Yorkie directly regulates the transcription of the Drosophila IκB homolog, Cactus, in Toll receptor-mediated antimicrobial response. Loss of Hippo pathway tumor suppressors or activation of Yorkie in fat bodies, the Drosophila immune organ, leads to elevated cactus mRNA levels, decreased expression of antimicrobial peptides, and vulnerability to infection by Gram-positive bacteria. Furthermore, Gram-positive bacteria acutely activate Hippo-Yorkie signaling in fat bodies via the Toll-Myd88-Pelle cascade through Pelle-mediated phosphorylation and degradation of the Cka subunit of the Hippo-inhibitory STRIPAK PP2A complex. Our studies elucidate a Toll-mediated Hippo signaling pathway in antimicrobial response, highlight the importance of regulating IκB/Cactus transcription in innate immunity, and identify Gram-positive bacteria as extracellular stimuli of Hippo signaling under physiological settings.

Indexed as

Immunity, InnateSignal TransductionAnimalsDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsEscherichia coliFat BodyHippo KinasesIntracellular Signaling Peptides and ProteinsLarvaMalePectobacterium carotovorumPhosphoproteinsProtein Serine-Threonine KinasesStaphylococcus aureuscact protein, DrosophilaDNA-Binding ProteinsDrosophila ProteinsHippo Kinaseshpo protein, DrosophilaIntracellular Signaling Peptides and ProteinsPhosphoproteinsProtein Serine-Threonine KinasesToll-Like Receptors

Identifiers

PMID26824654
PMCPMC4733248
OpenAlexW2266822253

What OpenQuestion 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 OpenQuestion graph.