Tsc2 is not a critical target of Akt during normal Drosophila development

Jixin Dong, Duojia Pan

Research output: Contribution to journalArticle

87 Citations (Scopus)

Abstract

Signaling by insulin and target of rapamycin are both required for cell growth, but their interrelationships remain poorly defined. It was reported that Akt, an essential component of the insulin pathway, stimulates growth by phosphorylating and inhibiting tuberous sclerosis complex 2 (TSC2). Here we evaluate this model genetically in Drosophila by engineering Tsc2 mutants in which the Akt phosphorylation sites are changed to nonphosphorylatable or phospho-mimicking residues. Strikingly, such mutants completely rescue the lethality and cell growth defects of Tsc2-null mutants. Taken together, our data suggest that Tsc2 is not a critical substrate of Akt in normal Drosophila development.

Original languageEnglish (US)
Pages (from-to)2479-2484
Number of pages6
JournalGenes and Development
Volume18
Issue number20
DOIs
StatePublished - Oct 15 2004

Fingerprint

Drosophila
Growth
Insulin
Tuberous Sclerosis
Sirolimus
Phosphorylation
Tuberous Sclerosis 2

Keywords

  • Cell growth
  • Insulin signaling
  • Target of rapamycin (TOR)
  • Tumor suppressor

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

Cite this

Tsc2 is not a critical target of Akt during normal Drosophila development. / Dong, Jixin; Pan, Duojia.

In: Genes and Development, Vol. 18, No. 20, 15.10.2004, p. 2479-2484.

Research output: Contribution to journalArticle

@article{28bf086fd709490aa2757ef70d82d0d7,
title = "Tsc2 is not a critical target of Akt during normal Drosophila development",
abstract = "Signaling by insulin and target of rapamycin are both required for cell growth, but their interrelationships remain poorly defined. It was reported that Akt, an essential component of the insulin pathway, stimulates growth by phosphorylating and inhibiting tuberous sclerosis complex 2 (TSC2). Here we evaluate this model genetically in Drosophila by engineering Tsc2 mutants in which the Akt phosphorylation sites are changed to nonphosphorylatable or phospho-mimicking residues. Strikingly, such mutants completely rescue the lethality and cell growth defects of Tsc2-null mutants. Taken together, our data suggest that Tsc2 is not a critical substrate of Akt in normal Drosophila development.",
keywords = "Cell growth, Insulin signaling, Target of rapamycin (TOR), Tumor suppressor",
author = "Jixin Dong and Duojia Pan",
year = "2004",
month = "10",
day = "15",
doi = "10.1101/gad.1240504",
language = "English (US)",
volume = "18",
pages = "2479--2484",
journal = "Genes and Development",
issn = "0890-9369",
publisher = "Cold Spring Harbor Laboratory Press",
number = "20",

}

TY - JOUR

T1 - Tsc2 is not a critical target of Akt during normal Drosophila development

AU - Dong, Jixin

AU - Pan, Duojia

PY - 2004/10/15

Y1 - 2004/10/15

N2 - Signaling by insulin and target of rapamycin are both required for cell growth, but their interrelationships remain poorly defined. It was reported that Akt, an essential component of the insulin pathway, stimulates growth by phosphorylating and inhibiting tuberous sclerosis complex 2 (TSC2). Here we evaluate this model genetically in Drosophila by engineering Tsc2 mutants in which the Akt phosphorylation sites are changed to nonphosphorylatable or phospho-mimicking residues. Strikingly, such mutants completely rescue the lethality and cell growth defects of Tsc2-null mutants. Taken together, our data suggest that Tsc2 is not a critical substrate of Akt in normal Drosophila development.

AB - Signaling by insulin and target of rapamycin are both required for cell growth, but their interrelationships remain poorly defined. It was reported that Akt, an essential component of the insulin pathway, stimulates growth by phosphorylating and inhibiting tuberous sclerosis complex 2 (TSC2). Here we evaluate this model genetically in Drosophila by engineering Tsc2 mutants in which the Akt phosphorylation sites are changed to nonphosphorylatable or phospho-mimicking residues. Strikingly, such mutants completely rescue the lethality and cell growth defects of Tsc2-null mutants. Taken together, our data suggest that Tsc2 is not a critical substrate of Akt in normal Drosophila development.

KW - Cell growth

KW - Insulin signaling

KW - Target of rapamycin (TOR)

KW - Tumor suppressor

UR - http://www.scopus.com/inward/record.url?scp=5444233787&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=5444233787&partnerID=8YFLogxK

U2 - 10.1101/gad.1240504

DO - 10.1101/gad.1240504

M3 - Article

VL - 18

SP - 2479

EP - 2484

JO - Genes and Development

JF - Genes and Development

SN - 0890-9369

IS - 20

ER -