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Inter-cell type interactions that control JNK signaling in the Drosophila intestine
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Inter-cell type interactions that control JNK signaling in the Drosophila intestine
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Journal Article
Inter-cell type interactions that control JNK signaling in the Drosophila intestine
2024
Overview
JNK signaling is a critical regulator of inflammation and regeneration, but how it is controlled in specific tissue contexts remains unclear. Here we show that, in the
Drosophila
intestine, the TNF-type ligand, Eiger (Egr), is expressed exclusively by intestinal stem cells (ISCs) and enteroblasts (EBs), where it is induced by stress and during aging. Egr preferentially activates JNK signaling in a paracrine fashion in differentiated enterocytes (ECs) via its receptor, Grindelwald (Grnd).
N
-glycosylation genes (
Alg3
,
Alg9
) restrain this activation, and stress-induced downregulation of
Alg3
and
Alg9
correlates with JNK activation, suggesting a regulatory switch. JNK activity in ECs induces expression of the intermembrane protease Rhomboid (Rho), driving secretion of EGFR ligands Keren (Krn) and Spitz (Spi), which in turn activate EGFR signaling in progenitor cells (ISCs and EBs) to stimulate their growth and division, as well as to produce more Egr. This study uncovers an
N
-glycosylation-controlled, paracrine JNK-EGFR-JNK feedforward loop that sustains ISC proliferation during stress-induced gut regeneration.
Zhang et al. illustrate a spatial activation pattern of JNK signaling within the intestinal stem cell lineage and uncover a paracrine JNK-EGFR-JNK feedforward loop that sustains ISC proliferation during stress-induced gut regeneration.
Publisher
Nature Publishing Group UK,Nature Portfolio
Subject
/ 38/39
/ 38/77
/ 38/89
/ 96/1
/ 96/100
/ 96/2
/ 96/31
/ 96/34
/ 96/95
/ Animals
/ Drosophila melanogaster - genetics
/ Drosophila melanogaster - metabolism
/ Drosophila Proteins - genetics
/ Drosophila Proteins - metabolism
/ Humanities and Social Sciences
/ Intestinal Mucosa - cytology
/ Intestinal Mucosa - metabolism
/ JNK Mitogen-Activated Protein Kinases - metabolism
/ Receptors, Invertebrate Peptide - genetics
/ Receptors, Invertebrate Peptide - metabolism
/ Science
