Nutrition-Responsive Glia Control Exit of Neural Stem Cells from Quiescence

The systemic regulation of stem cells ensures that they meet the needs of the organism during growth and in response to injury. A key point of regulation is the decision between quiescence and proliferation. During development, Drosophila neural stem cells (neuroblasts) transit through a period of q...

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Published in:Cell Vol. 143; no. 7; pp. 1161 - 1173
Main Authors: Chell, James M., Brand, Andrea H.
Format: Journal Article
Language:English
Published: United States Elsevier Inc 23-12-2010
Elsevier
Cell Press
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Abstract The systemic regulation of stem cells ensures that they meet the needs of the organism during growth and in response to injury. A key point of regulation is the decision between quiescence and proliferation. During development, Drosophila neural stem cells (neuroblasts) transit through a period of quiescence separating distinct embryonic and postembryonic phases of proliferation. It is known that neuroblasts exit quiescence via a hitherto unknown pathway in response to a nutrition-dependent signal from the fat body. We have identified a population of glial cells that produce insulin/IGF-like peptides in response to nutrition, and we show that the insulin/IGF receptor pathway is necessary for neuroblasts to exit quiescence. The forced expression of insulin/IGF-like peptides in glia, or activation of PI3K/Akt signaling in neuroblasts, can drive neuroblast growth and proliferation in the absence of dietary protein and thus uncouple neuroblasts from systemic control. [Display omitted] ► Stellate glia express insulin/IGF-like peptides (dILPs) in response to nutrition ► Insulin receptor/PI3K signaling is required for neural stem cell (NSC) reactivation ► Glial dILP expression is sufficient to reactivate NSCs irrespective of nutrition ► Glial signaling is essential for NSC exit from quiescence
AbstractList The systemic regulation of stem cells ensures that they meet the needs of the organism during growth and in response to injury. A key point of regulation is the decision between quiescence and proliferation. During development, Drosophila neural stem cells (neuroblasts) transit through a period of quiescence separating distinct embryonic and postembryonic phases of proliferation. It is known that neuroblasts exit quiescence via a hitherto unknown pathway in response to a nutrition-dependent signal from the fat body. We have identified a population of glial cells that produce insulin/IGF-like peptides in response to nutrition, and we show that the insulin/IGF receptor pathway is necessary for neuroblasts to exit quiescence. The forced expression of insulin/IGF-like peptides in glia, or activation of PI3K/Akt signaling in neuroblasts, can drive neuroblast growth and proliferation in the absence of dietary protein and thus uncouple neuroblasts from systemic control.
The systemic regulation of stem cells ensures that they meet the needs of the organism during growth and in response to injury. A key point of regulation is the decision between quiescence and proliferation. During development, Drosophila neural stem cells (neuroblasts) transit through a period of quiescence separating distinct embryonic and postembryonic phases of proliferation. It is known that neuroblasts exit quiescence via a hitherto unknown pathway in response to a nutrition-dependent signal from the fat body. We have identified a population of glial cells that produce insulin/IGF-like peptides in response to nutrition, and we show that the insulin/IGF receptor pathway is necessary for neuroblasts to exit quiescence. The forced expression of insulin/IGF-like peptides in glia, or activation of PI3K/Akt signaling in neuroblasts, can drive neuroblast growth and proliferation in the absence of dietary protein and thus uncouple neuroblasts from systemic control. [Display omitted] ► Stellate glia express insulin/IGF-like peptides (dILPs) in response to nutrition ► Insulin receptor/PI3K signaling is required for neural stem cell (NSC) reactivation ► Glial dILP expression is sufficient to reactivate NSCs irrespective of nutrition ► Glial signaling is essential for NSC exit from quiescence
The systemic regulation of stem cells ensures that they meet the needs of the organism during growth and in response to injury. A key point of regulation is the decision between quiescence and proliferation. During development, Drosophila neural stem cells (neuroblasts) transit through a period of quiescence separating distinct embryonic and postembryonic phases of proliferation. It is known that neuroblasts exit quiescence via a hitherto unknown pathway in response to a nutrition-dependent signal from the fat body. We have identified a population of glial cells that produce insulin/IGF-like peptides in response to nutrition, and we show that the insulin/IGF receptor pathway is necessary for neuroblasts to exit quiescence. The forced expression of insulin/IGF-like peptides in glia, or activation of PI3K/Akt signaling in neuroblasts, can drive neuroblast growth and proliferation in the absence of dietary protein and thus uncouple neuroblasts from systemic control.
The systemic regulation of stem cells ensures that they meet the needs of the organism during growth and in response to injury. A key point of regulation is the decision between quiescence and proliferation. During development, Drosophila neural stem cells (neuroblasts) transit through a period of quiescence separating distinct embryonic and postembryonic phases of proliferation. It is known that neuroblasts exit quiescence via a hitherto unknown pathway in response to a nutrition-dependent signal from the fat body. We have identified a population of glial cells that produce insulin/IGF-like peptides in response to nutrition, and we show that the insulin/IGF receptor pathway is necessary for neuroblasts to exit quiescence. The forced expression of insulin/IGF-like peptides in glia, or activation of PI3K/Akt signaling in neuroblasts, can drive neuroblast growth and proliferation in the absence of dietary protein and thus uncouple neuroblasts from systemic control.
Author Brand, Andrea H.
Chell, James M.
AuthorAffiliation 1 The Gurdon Institute and Department of Physiology, Development, and Neuroscience, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
AuthorAffiliation_xml – name: 1 The Gurdon Institute and Department of Physiology, Development, and Neuroscience, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
Author_xml – sequence: 1
  givenname: James M.
  surname: Chell
  fullname: Chell, James M.
  organization: The Gurdon Institute and Department of Physiology, Development, and Neuroscience, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
– sequence: 2
  givenname: Andrea H.
  surname: Brand
  fullname: Brand, Andrea H.
  email: ahb@mole.bio.cam.ac.uk
  organization: The Gurdon Institute and Department of Physiology, Development, and Neuroscience, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
BackLink https://www.ncbi.nlm.nih.gov/pubmed/21183078$$D View this record in MEDLINE/PubMed
https://www.osti.gov/biblio/1623640$$D View this record in Osti.gov
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Snippet The systemic regulation of stem cells ensures that they meet the needs of the organism during growth and in response to injury. A key point of regulation is...
The systemic regulation of stem cells ensures that they meet the needs of the organism during growth and in response to injury. A key point of regulation is...
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Index Database
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StartPage 1161
SubjectTerms Animals
BASIC BIOLOGICAL SCIENCES
Biochemistry & Molecular Biology
Cell Biology
Diet
Drosophila
Drosophila - cytology
Drosophila - embryology
Drosophila - metabolism
Fat Body - metabolism
Gene Expression Regulation, Developmental
Neural Stem Cells - cytology
Neuroglia - cytology
Somatomedins - metabolism
Title Nutrition-Responsive Glia Control Exit of Neural Stem Cells from Quiescence
URI https://dx.doi.org/10.1016/j.cell.2010.12.007
https://www.ncbi.nlm.nih.gov/pubmed/21183078
https://search.proquest.com/docview/821199054
https://search.proquest.com/docview/869588138
https://www.osti.gov/biblio/1623640
https://pubmed.ncbi.nlm.nih.gov/PMC3087489
Volume 143
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