Jonathan O. Lipton
First author of the two studies that tie mTOR signalling to the circadian clock protein BMAL1: S6K1 phosphorylates BMAL1 to drive translation, and constant mTOR activity in tuberous sclerosis disturbs the clock.
Assistant Professor of Neurology, Boston Children's Hospital and Harvard Medical School · postdoc with Mustafa Sahin, Boston Children's Hospital; clinical training in child neurology and sleep medicine (Boston Children's / Beth Israel Deaconess) · MD, PhD, Albert Einstein College of Medicine (Scott Emmons lab)
Lipton Lab, F.M. Kirby Neurobiology Center, Department of Neurology, Boston Children's Hospital and Harvard Medical School (Boston, Massachusetts, USA) ↗ Lab lineagetrained under Mustafa Sahin →
Portrait: Lipton Lab
As first author in Mustafa Sahin's lab, Lipton showed that S6K1, a main output of mTORC1, phosphorylates the clock protein BMAL1 at serine 42, which lets BMAL1 bind the translation machinery and drive daily rhythms of protein synthesis (LIP2015). Two years later his team found that mouse models of tuberous sclerosis, where mTOR is always on, keep abnormally high BMAL1 levels and have disturbed circadian behaviour, and that lowering BMAL1 restored the rhythms (LIP2017).
Lipton studied Classics at Brown University and did his MD/PhD at Albert Einstein College of Medicine, with a thesis on the genetics of motivated behaviour in Scott Emmons' lab. He trained in child neurology and sleep medicine in Boston, and his lab at Boston Children's Hospital now studies how circadian clocks relate to diseases of the developing brain.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2015 | A | The Circadian Protein BMAL1 Regulates Translation in Response to S6K1-Mediated Phosphorylation LIP2015 First author: S6K1 phosphorylates BMAL1, which then promotes translation and links mTOR to circadian protein synthesis. |
| 2017 | A | Aberrant Proteostasis of BMAL1 Underlies Circadian Abnormalities in a Paradigmatic mTOR-opathy LIP2017 First and corresponding author: mTOR overactivity in tuberous sclerosis models raises BMAL1 and disrupts circadian rhythms. |
Co-authors in the Atlas
People with a profile here who share at least one study with Jonathan O. Lipton.
- Ashwin Nathan 2 shared studies Co-author on both Boston Children's Hospital studies linking mTOR signalling to the circadian clock protein BMAL1.
- Elizabeth D. Yuan 2 shared studies Second author on the study showing that S6K1 phosphorylates BMAL1 to link mTOR signalling with circadian protein synthesis, and co-author on the follow-up in tuberous sclerosis models.
- Fred C. Davis 2 shared studies Circadian biologist from Northeastern University who brought expertise on the brain's master clock to two studies linking mTOR and the clock protein BMAL1.
- Lara M. Boyle 2 shared studies Research assistant at Boston Children's Hospital who co-authored both studies linking mTOR to the clock protein BMAL1, including the tuberous sclerosis study where she was second author.
- Mustafa Sahin 2 shared studies Senior author of the studies showing that mTOR signalling reaches the circadian clock through BMAL1, and a physician-scientist focused on tuberous sclerosis, the classic disease of overactive mTOR.
- John M. Asara Mass-spectrometry specialist whose core facility supplied metabolomics and proteomics for several mTOR studies, including measurements of purine, pyrimidine and SAM metabolism downstream of mTORC1.
Every researcher with a profile →
Thank you. Your answer was counted anonymously.
Thank you. That helps us know which pages have been read by someone who knows the work.
Thank you. We will check it and correct the page.