Drosophila activins adapt gut size to food intake and promote regenerative growth

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Drosophila activins adapt gut size to food intake and promote regenerative growth. / Christensen, Christian F.; Laurichesse, Quentin; Loudhaief, Rihab; Colombani, Julien; Andersen, Ditte S.

In: Nature Communications, Vol. 15, No. 1, 273, 2024.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Christensen, CF, Laurichesse, Q, Loudhaief, R, Colombani, J & Andersen, DS 2024, 'Drosophila activins adapt gut size to food intake and promote regenerative growth', Nature Communications, vol. 15, no. 1, 273. https://doi.org/10.1038/s41467-023-44553-9

APA

Christensen, C. F., Laurichesse, Q., Loudhaief, R., Colombani, J., & Andersen, D. S. (2024). Drosophila activins adapt gut size to food intake and promote regenerative growth. Nature Communications, 15(1), [273]. https://doi.org/10.1038/s41467-023-44553-9

Vancouver

Christensen CF, Laurichesse Q, Loudhaief R, Colombani J, Andersen DS. Drosophila activins adapt gut size to food intake and promote regenerative growth. Nature Communications. 2024;15(1). 273. https://doi.org/10.1038/s41467-023-44553-9

Author

Christensen, Christian F. ; Laurichesse, Quentin ; Loudhaief, Rihab ; Colombani, Julien ; Andersen, Ditte S. / Drosophila activins adapt gut size to food intake and promote regenerative growth. In: Nature Communications. 2024 ; Vol. 15, No. 1.

Bibtex

@article{5def4ef1720a4db7aafa8657763353a6,
title = "Drosophila activins adapt gut size to food intake and promote regenerative growth",
abstract = "Rapidly renewable tissues adapt different strategies to cope with environmental insults. While tissue repair is associated with increased intestinal stem cell (ISC) proliferation and accelerated tissue turnover rates, reduced calorie intake triggers a homeostasis-breaking process causing adaptive resizing of the gut. Here we show that activins are key drivers of both adaptive and regenerative growth. Activin-β (Actβ) is produced by stem and progenitor cells in response to intestinal infections and stimulates ISC proliferation and turnover rates to promote tissue repair. Dawdle (Daw), a divergent Drosophila activin, signals through its receptor, Baboon, in progenitor cells to promote their maturation into enterocytes (ECs). Daw is dynamically regulated during starvation-refeeding cycles, where it couples nutrient intake with progenitor maturation and adaptive resizing of the gut. Our results highlight an activin-dependent mechanism coupling nutrient intake with progenitor-to-EC maturation to promote adaptive resizing of the gut and further establish activins as key regulators of adult tissue plasticity.",
author = "Christensen, {Christian F.} and Quentin Laurichesse and Rihab Loudhaief and Julien Colombani and Andersen, {Ditte S.}",
note = "Publisher Copyright: {\textcopyright} 2024, The Author(s).",
year = "2024",
doi = "10.1038/s41467-023-44553-9",
language = "English",
volume = "15",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",
number = "1",

}

RIS

TY - JOUR

T1 - Drosophila activins adapt gut size to food intake and promote regenerative growth

AU - Christensen, Christian F.

AU - Laurichesse, Quentin

AU - Loudhaief, Rihab

AU - Colombani, Julien

AU - Andersen, Ditte S.

N1 - Publisher Copyright: © 2024, The Author(s).

PY - 2024

Y1 - 2024

N2 - Rapidly renewable tissues adapt different strategies to cope with environmental insults. While tissue repair is associated with increased intestinal stem cell (ISC) proliferation and accelerated tissue turnover rates, reduced calorie intake triggers a homeostasis-breaking process causing adaptive resizing of the gut. Here we show that activins are key drivers of both adaptive and regenerative growth. Activin-β (Actβ) is produced by stem and progenitor cells in response to intestinal infections and stimulates ISC proliferation and turnover rates to promote tissue repair. Dawdle (Daw), a divergent Drosophila activin, signals through its receptor, Baboon, in progenitor cells to promote their maturation into enterocytes (ECs). Daw is dynamically regulated during starvation-refeeding cycles, where it couples nutrient intake with progenitor maturation and adaptive resizing of the gut. Our results highlight an activin-dependent mechanism coupling nutrient intake with progenitor-to-EC maturation to promote adaptive resizing of the gut and further establish activins as key regulators of adult tissue plasticity.

AB - Rapidly renewable tissues adapt different strategies to cope with environmental insults. While tissue repair is associated with increased intestinal stem cell (ISC) proliferation and accelerated tissue turnover rates, reduced calorie intake triggers a homeostasis-breaking process causing adaptive resizing of the gut. Here we show that activins are key drivers of both adaptive and regenerative growth. Activin-β (Actβ) is produced by stem and progenitor cells in response to intestinal infections and stimulates ISC proliferation and turnover rates to promote tissue repair. Dawdle (Daw), a divergent Drosophila activin, signals through its receptor, Baboon, in progenitor cells to promote their maturation into enterocytes (ECs). Daw is dynamically regulated during starvation-refeeding cycles, where it couples nutrient intake with progenitor maturation and adaptive resizing of the gut. Our results highlight an activin-dependent mechanism coupling nutrient intake with progenitor-to-EC maturation to promote adaptive resizing of the gut and further establish activins as key regulators of adult tissue plasticity.

U2 - 10.1038/s41467-023-44553-9

DO - 10.1038/s41467-023-44553-9

M3 - Journal article

C2 - 38177201

AN - SCOPUS:85181523208

VL - 15

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

IS - 1

M1 - 273

ER -

ID: 379651166