title: Apoptosis restores cellular density by eliminating a physiologically or genetically induced excess of enterocytes in theDrosophilamidgut.
abstract: Using pathogens or high levels of opportunistic bacteria to damage the gut, studies inDrosophilahave identified many signaling pathways involved in gut regeneration. Dying cells emit signaling molecules that accelerate intestinal stem cell proliferation and progenitor differentiation to replace the dying cells quickly. This process has been named 'regenerative cell death'. Here, mimicking environmental conditions, we show that the ingestion of low levels of opportunistic bacteria was sufficient to launch an accelerated cellular renewal program despite the brief passage of bacteria in the gut and the absence of cell death and this is is due to the moderate induction of the JNK pathway that stimulates stem cell proliferation. Consequently, the addition of new differentiated cells to the gut epithelium, without preceding cell loss, leads to enterocyte overcrowding. Finally, we show that a couple of days later, the correct density of enterocytes is promptly restored by means of a wave of apoptosis involving Hippo signaling and preferential removal of old enterocytes.
authors.affiliation: Université Côte d'Azur, INRA, CNRS, ISA, 06900 Sophia Antipolis, France.
authors.forename: Rihab
authors.initials: R
authors.lastname: Loudhaief
authors.affiliation: Université Côte d'Azur, INRA, CNRS, ISA, 06900 Sophia Antipolis, France.
authors.forename: Alexandra
authors.initials: A
authors.lastname: Brun-Barale
authors.affiliation: Université Côte d'Azur, INRA, CNRS, ISA, 06900 Sophia Antipolis, France.
authors.forename: Olivia
authors.initials: O
authors.lastname: Benguettat
authors.affiliation: Université Côte d'Azur, INRA, CNRS, ISA, 06900 Sophia Antipolis, France.
authors.forename: Marie-Paule
authors.initials: MP
authors.lastname: Nawrot-Esposito
authors.affiliation: Université Côte d'Azur, INRA, CNRS, ISA, 06900 Sophia Antipolis, France.
authors.forename: David
authors.initials: D
authors.lastname: Pauron
authors.affiliation: Université Côte d'Azur, INRA, CNRS, ISA, 06900 Sophia Antipolis, France.
authors.forename: Marcel
authors.initials: M
authors.lastname: Amichot
authors.affiliation: Université Côte d'Azur, INRA, CNRS, ISA, 06900 Sophia Antipolis, France gallet@unice.fr.
authors.forename: Armel
authors.initials: A
authors.lastname: Gallet
mesh_terms: D000818:Animals; D017209:Apoptosis; D016923:Cell Death; D002454:Cell Differentiation / Q000502:physiology; D049109:Cell Proliferation; D016207:Cytokines / Q000378:metabolism; D029721:Drosophila Proteins / Q000378:metabolism; D004331:Drosophila melanogaster / Q000254:growth & development*; D004707:Endoderm / Q000166:cytology; D020895:Enterocytes / Q000166:cytology*; D004848:Epithelium / Q000254:growth & development; D005260:Female; D049452:Green Fluorescent Proteins / Q000378:metabolism; D006706:Homeostasis; D007422:Intestines / Q000254:growth & development*; D012038:Regeneration; D015398:Signal Transduction; D013234:Stem Cells / Q000166:cytology
chemical_list: D016207:Cytokines; D029721:Drosophila Proteins; D049452:Green Fluorescent Proteins
keywords: Apoptosis; Cellular homeostasis; Drosophila intestine; Hippo signaling; JNK signaling; Opportunistic bacteria