Research ArticleCellular Metabolism

PIP4kγ is a substrate for mTORC1 that maintains basal mTORC1 signaling during starvation

See allHide authors and affiliations

Science Signaling  04 Nov 2014:
Vol. 7, Issue 350, pp. ra104
DOI: 10.1126/scisignal.2005191

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Maintaining a Basal Level of Activity

Nutrients such as glucose and amino acids activate mammalian target of rapamycin complex 1 (mTORC1), a complex consisting of the kinase mTOR, which couples metabolic signals to pathways that trigger cellular proliferation and growth. When nutrients are limiting, mTORC1 activity is normally suppressed. Mackey et al. found that under nutrient-depleted conditions, the kinase PIP4kγ interacted with and activated mTORC1, which stimulated mTOR kinase activity at low levels. Under nutrient-replete conditions, mTOR phosphorylated PIP4kγ, inhibiting this pathway. Thus, PIP4kγ and mTORC1 exist in a feedback loop that ensures basal activity of mTORC1 during starvation and that is shut down when nutrients become available again.

View Full Text

Stay Connected to Science Signaling