SMG-1 and mTORC1 act antagonistically to regulate response to injury and growth in planarians.

Planarian flatworms are able to both regenerate their whole bodies and continuously adapt their size to nutrient status. Tight control of stem cell proliferation and differentiation during these processes is the key feature of planarian biology. Here we show that the planarian homolog of the phospho...

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Main Authors: Cristina González-Estévez, Daniel A Felix, Matthew D Smith, Jordi Paps, Simon J Morley, Victoria James, Tyson V Sharp, A Aziz Aboobaker
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS Genetics
Online Access:https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1002619&type=printable
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author Cristina González-Estévez
Daniel A Felix
Matthew D Smith
Jordi Paps
Simon J Morley
Victoria James
Tyson V Sharp
A Aziz Aboobaker
author_facet Cristina González-Estévez
Daniel A Felix
Matthew D Smith
Jordi Paps
Simon J Morley
Victoria James
Tyson V Sharp
A Aziz Aboobaker
author_sort Cristina González-Estévez
collection DOAJ
description Planarian flatworms are able to both regenerate their whole bodies and continuously adapt their size to nutrient status. Tight control of stem cell proliferation and differentiation during these processes is the key feature of planarian biology. Here we show that the planarian homolog of the phosphoinositide 3-kinase-related kinase (PIKK) family member SMG-1 and mTOR complex 1 components are required for this tight control. Loss of smg-1 results in a hyper-responsiveness to injury and growth and the formation of regenerative blastemas that remain undifferentiated and that lead to lethal ectopic outgrowths. Invasive stem cell hyper-proliferation, hyperplasia, hypertrophy, and differentiation defects are hallmarks of this uncontrolled growth. These data imply a previously unappreciated and novel physiological function for this PIKK family member. In contrast we found that planarian members of the mTOR complex 1, tor and raptor, are required for the initial response to injury and blastema formation. Double smg-1 RNAi experiments with tor or raptor show that abnormal growth requires mTOR signalling. We also found that the macrolide rapamycin, a natural compound inhibitor of mTORC1, is able to increase the survival rate of smg-1 RNAi animals by decreasing cell proliferation. Our findings support a model where Smg-1 acts as a novel regulator of both the response to injury and growth control mechanisms. Our data suggest the possibility that this may be by suppressing mTOR signalling. Characterisation of both the planarian mTORC1 signalling components and another PIKK family member as key regulators of regeneration and growth will influence future work on regeneration, growth control, and the development of anti-cancer therapies that target mTOR signalling.
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spelling doaj-art-bf3c1da8bcdb470b8094fc4192252b8e2025-08-20T02:30:59ZengPublic Library of Science (PLoS)PLoS Genetics1553-73901553-74042012-01-0183e100261910.1371/journal.pgen.1002619SMG-1 and mTORC1 act antagonistically to regulate response to injury and growth in planarians.Cristina González-EstévezDaniel A FelixMatthew D SmithJordi PapsSimon J MorleyVictoria JamesTyson V SharpA Aziz AboobakerPlanarian flatworms are able to both regenerate their whole bodies and continuously adapt their size to nutrient status. Tight control of stem cell proliferation and differentiation during these processes is the key feature of planarian biology. Here we show that the planarian homolog of the phosphoinositide 3-kinase-related kinase (PIKK) family member SMG-1 and mTOR complex 1 components are required for this tight control. Loss of smg-1 results in a hyper-responsiveness to injury and growth and the formation of regenerative blastemas that remain undifferentiated and that lead to lethal ectopic outgrowths. Invasive stem cell hyper-proliferation, hyperplasia, hypertrophy, and differentiation defects are hallmarks of this uncontrolled growth. These data imply a previously unappreciated and novel physiological function for this PIKK family member. In contrast we found that planarian members of the mTOR complex 1, tor and raptor, are required for the initial response to injury and blastema formation. Double smg-1 RNAi experiments with tor or raptor show that abnormal growth requires mTOR signalling. We also found that the macrolide rapamycin, a natural compound inhibitor of mTORC1, is able to increase the survival rate of smg-1 RNAi animals by decreasing cell proliferation. Our findings support a model where Smg-1 acts as a novel regulator of both the response to injury and growth control mechanisms. Our data suggest the possibility that this may be by suppressing mTOR signalling. Characterisation of both the planarian mTORC1 signalling components and another PIKK family member as key regulators of regeneration and growth will influence future work on regeneration, growth control, and the development of anti-cancer therapies that target mTOR signalling.https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1002619&type=printable
spellingShingle Cristina González-Estévez
Daniel A Felix
Matthew D Smith
Jordi Paps
Simon J Morley
Victoria James
Tyson V Sharp
A Aziz Aboobaker
SMG-1 and mTORC1 act antagonistically to regulate response to injury and growth in planarians.
PLoS Genetics
title SMG-1 and mTORC1 act antagonistically to regulate response to injury and growth in planarians.
title_full SMG-1 and mTORC1 act antagonistically to regulate response to injury and growth in planarians.
title_fullStr SMG-1 and mTORC1 act antagonistically to regulate response to injury and growth in planarians.
title_full_unstemmed SMG-1 and mTORC1 act antagonistically to regulate response to injury and growth in planarians.
title_short SMG-1 and mTORC1 act antagonistically to regulate response to injury and growth in planarians.
title_sort smg 1 and mtorc1 act antagonistically to regulate response to injury and growth in planarians
url https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1002619&type=printable
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