Evidence map›Paper›PMID 35950466›Full record

ArticleThe EMBO journal2022

Damage-induced regeneration of the intestinal stem cell pool through enteroblast mitosis in the Drosophila midgut.

Aiguo Tian, Virginia Morejon, Sarah Kohoutek, Yi-Chun Huang, Wu-Min Deng, Jin Jiang

Abstract read
In one paragraph

Article in The EMBO journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Evidence that injury can causebioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Drosophila Intestine as a Model to Study Tumors.Advances in experimental medicine and biology · 2025
    Review
  9. Host-Microbe Interactions in Drosophila Cancer.Advances in experimental medicine and biology · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
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

6 authors.

Aiguo TianDepartment of Biochemistry and Molecular Biology, Tulane University School of Medicine, Louisiana Cancer Research Center, New Orleans, LA, USA.ORCID 0000-0001-5011-6034
Virginia MorejonDepartment of Biochemistry and Molecular Biology, Tulane University School of Medicine, Louisiana Cancer Research Center, New Orleans, LA, USA.
Sarah KohoutekDepartment of Biochemistry and Molecular Biology, Tulane University School of Medicine, Louisiana Cancer Research Center, New Orleans, LA, USA.
Yi-Chun HuangDepartment of Biochemistry and Molecular Biology, Tulane University School of Medicine, Louisiana Cancer Research Center, New Orleans, LA, USA.ORCID 0000-0001-6409-485X
Wu-Min DengDepartment of Biochemistry and Molecular Biology, Tulane University School of Medicine, Louisiana Cancer Research Center, New Orleans, LA, USA.
Jin JiangDepartment of Molecular Biology and Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID 0000-0002-5951-372X

Funding

The role of the CMV-associated reactive oxygen species in age-relatedP20GM103629 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI ROUT, NAMITA · 2012 to 2021
$22.4M
Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Cell signaling in development and regenerationR35GM118063 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI Jin Jiang · 2016 to 2026
$9.4M
Notch signaling and germline-soma interactions in the Drosophila ovarian modelR01GM072562 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI DENG, WU-MIN · 2006 to 2025
$5.6M
Tissue Microenvironment ant Tumor Hotspots in DrosophilaR01CA227789 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI DENG, WU-MIN · 2019 to 2023
$1.7M
Mechanistic investigation of malignant rhabdoid childhood tumor using the Drosophila modelR01CA224381 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI DENG, WU-MIN · 2018 to 2022
$1.7M
NCI NIH HHS R01 CA224381NCI NIH HHS R01 CA227789NIGMS NIH HHS P20 GM103629NIGMS NIH HHS R01 GM072562NIGMS NIH HHS R35 GM118063NIH HHS P40 OD018537
6 · The paper itself

Abstract

Many adult tissues and organs including the intestine rely on resident stem cells to maintain homeostasis and regeneration. In mammals, the progenies of intestinal stem cells (ISCs) can dedifferentiate to generate ISCs upon ablation of resident stem cells. However, whether and how mature tissue cells generate ISCs under physiological conditions remains unknown. Here, we show that infection of the Drosophila melanogaster intestine with pathogenic bacteria induces entry of enteroblasts (EBs), which are ISC progenies, into the mitotic cycle through upregulation of epidermal growth factor receptor (EGFR)-Ras signaling. We also show that ectopic activation of EGFR-Ras signaling in EBs is sufficient to drive enteroblast mitosis cell autonomously. Furthermore, we find that the dividing enteroblasts do not gain ISC identity as a prerequisite to divide, and the regenerative ISCs are produced through EB mitosis. Taken together, our work uncovers a new role for EGFR-Ras signaling in driving EB mitosis and replenishing the ISC pool during fly intestinal regeneration, which may have important implications for tissue homeostasis and tumorigenesis in vertebrates.

Indexed as

DrosophilaDrosophila ProteinsAnimalsCell ProliferationDrosophila melanogasterErbB ReceptorsIntestinesMammalsMitosisStem CellsDrosophila ProteinsErbB ReceptorsdedifferentiationDrosophila midgutenteroblastsregenerationstem cells

Identifiers

PMID35950466
PMCPMC9531297

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.