Maya P. Byfield
Showed as first author that the lipid kinase hVps34 is regulated by nutrients and is needed for amino acids to activate S6 kinase through mTOR, in parallel with a study from George Thomas's group
Professor of Biology, Seminole State College of Florida · postdoc, Burnett School of Biomedical Sciences, University of Central Florida · PhD in Molecular Pharmacology, Albert Einstein College of Medicine
Portrait: Seminole State College of Florida
BYF2005 does something unusual for its year: it separates two inputs that were being treated as one. Insulin reaches S6K1 through class I PI3K and Akt. Byfield showed that the class III PI 3-kinase hVps34 also sits upstream of S6K1, is required for the phosphorylation of both S6K1 and 4E-BP1, and yet is not part of the insulin arm at all — knocking it down leaves Akt and TSC2 phosphorylation untouched.
What makes hVps34 a candidate for the nutrient arm is how it behaves: it is switched off by amino acid or glucose starvation, and by activating AMPK. That is the profile of something reporting on supply rather than on hormones. The paper is careful about the limit of this — the sensor itself is not identified, and the evidence is knockdown, overexpression and antibody microinjection in cell lines.
After her PhD at Einstein she did a neuroscience postdoc at the University of Central Florida and then moved into teaching, as a professor of biology at Seminole State College of Florida, where she also founded the Phenomenal STEM(ist) outreach initiative.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2005 | M | hVps34 is a nutrient-regulated lipid kinase required for activation of p70 S6 kinase BYF2005 First author: hVps34 is inhibited by amino acid and glucose starvation and is required for S6K1 activation, outside the insulin/class I PI3K route. |
| 2005 | M | Amino acids mediate mTOR/raptor signaling through activation of class 3 phosphatidylinositol 3OH-kinase NOB2005 The companion paper to BYF2005, from a different laboratory: the amino acid input to mTORC1 is separate from the insulin input and runs through class 3 PI3K (hVps34), not through class 1 PI3K. Historically important because it states that the amino acid branch is the older one and that insulin signalling was grafted onto it. Boundary: cell lines, pharmacological and knockdown evidence; the later Rag/Ragulator account describes a different route to the same target, and the two accounts are not reconciled in the work this Atlas holds. |
Co-authors in the Atlas 3
People with a profile here who share at least one study with Maya P. Byfield.
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- Jonathan M. Backer 2 shared studies Showed that the class III PI 3-kinase hVps34, best known for its role in autophagy, is regulated by nutrients and is needed for amino acids to activate S6 kinase through mTOR, in parallel with George Thomas's group
- Johannes L. (Hans) Bos Cancer biologist known for work on Ras mutations and for the small GTPase Rap1 and its activator Epac, a cAMP-regulated switch for cell adhesion
- Takahiro Nobukuni Showed as first author that amino acids activate mTOR through the lipid kinase hVps34, by a route separate from insulin signalling through TSC, in parallel with a study from Jonathan Backer's laboratory
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