Nutritional regulation of neural stem cell reactivation in Drosophila melanogaster
type: CreativeWork
description: In order to coordinate brain development with the growth of the organism, neurogenesis is highly dependent on the organism’s nutritional intake. The transition between neural stem cell (NSC) quiescence and reactivation is a key point of regulation during neurogenesis, and in Drosophila, this process is tightly coupled to nutrient availability. Post-embryonic NSCs in Drosophila only exit quiescence when larvae are fed a diet containing essential amino acids. The fat body, a functional homologue of the liver and adipose tissue, acts as a systemic nutrient sensor. Existing evidence from both in vivo and in vitro studies suggest that upon sensing dietary amino acids, the fat body secretes unknown factor(s) that induce glial secretion of insulin/IGF-peptides, which are sensed by underlying NSCs to trigger their reactivation. Despite recent work on nutritional regulation of NSC reactivation, key questions still remain: what are the signal(s) from the fat body, and how do they interact with the glial cells to induce glial production of DIlps? In addition, a number of glial subtypes are closely associated with the NSCs, but each subtype’s individual contribution to NSC reactivation remains elusive. In order to search for the unknown fat body factor(s) and investigate how they interact with the glial cells, I compared the transcriptome of the fat body under fed and starvation conditions during the time window of NSC reactivation. I identified an extracellular matrix protein (ECM), Collagen IV, as a secreted fat body signal whose deposition on the CNS is required for NSC reactivation. Collagen IV recruits glial-derived Perlecan, an- other ECM protein and a known requirement for NSC reactivation, to the vicinity of NSCs. Both ECM proteins are indispensable for the induction of glial insulin/IGF signalling. NSCs are separated from the hemolymph by a blood brain barrier (BBB). In collaboration with Pauline Speder and Jessie Van Buggenum (Andrea Brand lab), we confirmed crucial r…
abstract: In order to coordinate brain development with the growth of the organism, neurogenesis is highly dependent on the organism’s nutritional intake. The transition between neural stem cell (NSC) quiescence and reactivation is a key point of regulation during neurogenesis, and in Drosophila, this process is tightly coupled to nutrient availability. Post-embryonic NSCs in Drosophila only exit quiescence when larvae are fed a diet containing essential amino acids. The fat body, a functional homologue of the liver and adipose tissue, acts as a systemic nutrient sensor. Existing evidence from both in vivo and in vitro studies suggest that upon sensing dietary amino acids, the fat body secretes unknown factor(s) that induce glial secretion of insulin/IGF-peptides, which are sensed by underlying NSCs to trigger their reactivation. Despite recent work on nutritional regulation of NSC reactivation, key questions still remain: what are the signal(s) from the fat body, and how do they interact with the glial cells to induce glial production of DIlps? In addition, a number of glial subtypes are closely associated with the NSCs, but each subtype’s individual contribution to NSC reactivation remains elusive. In order to search for the unknown fat body factor(s) and investigate how they interact with the glial cells, I compared the transcriptome of the fat body under fed and starvation conditions during the time window of NSC reactivation. I identified an extracellular matrix protein (ECM), Collagen IV, as a secreted fat body signal whose deposition on the CNS is required for NSC reactivation. Collagen IV recruits glial-derived Perlecan, an- other ECM protein and a known requirement for NSC reactivation, to the vicinity of NSCs. Both ECM proteins are indispensable for the induction of glial insulin/IGF signalling. NSCs are separated from the hemolymph by a blood brain barrier (BBB). In collaboration with Pauline Speder and Jessie Van Buggenum (Andrea Brand lab), we confirmed crucial r…
author: Liu, Jun
language: en
license: https://apollo8-f-pro.lib.cam.ac.uk/bitstreams/de51e192-ee7d-4639-b5bd-5f09ba99847c/download
license: https://www.rioxx.net/licenses/all-rights-reserved/
date published: 2015-06-09
date modified: 2026-07-22T22:24:18Z
provider: Cambridge University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: University of Cambridge

PropertyValue
property ID: DOI
value: 10.17863/CAM.16342