Mondira Kundu
Physician-scientist who works out what the autophagy-initiating kinases ULK1 and ULK2 actually do when a cell runs short of fuel
Member, Department of Cell and Molecular Biology, St. Jude Children's Research Hospital · Faculty, Department of Pathology, St. Jude Children's Research Hospital · Research training, Department of Pathology and Laboratory Medicine, University of Pennsylvania · Clinical Pathology Residency and Hematopathology Fellowship, Hospital of the University of Pennsylvania · Postdoctoral Fellow, NHGRI / NIH · MD and PhD, Jefferson Medical College · BS, Pennsylvania State University · Elected member, American Society for Clinical Investigation (2017)
Kundu Lab, St. Jude Children's Research Hospital (Memphis, Tennessee, USA) ↗
Portrait: St. Jude Children's Research Hospital
KIM2011 showed that ULK1, the kinase that starts autophagy, is a switch with two hands on it. When glucose runs out, AMPK phosphorylates ULK1 at Ser317 and Ser777 and switches it on; when nutrients are plentiful, mTORC1 phosphorylates Ser757, which both keeps ULK1 quiet and physically peels AMPK off it. Kundu is the second author, and the Ulk1-knockout mouse cells in which the paper's rescue experiments are done come out of her own work on the kinase.
Three years earlier she had shown what ULK1 is for in an animal. A maturing red blood cell has to dispose of its mitochondria and ribosomes before it becomes an erythrocyte, and Kundu found that Ulk1-null mice fail at precisely that step - yet ordinary starvation-induced autophagy still worked in them. ULK1 therefore belongs to the selective clearance machinery rather than being a core requirement for autophagy itself.
She trained as a physician first: MD and PhD at Jefferson Medical College, then clinical pathology and hematopathology at the University of Pennsylvania, with postdoctoral research at the NIH and at Penn. Her lab at St. Jude now studies ULK1 and ULK2 as coordinators of the metabolic stress response and somatic mitochondrial DNA mutations, including recent work on how glucose starvation reroutes traffic from the ER to the Golgi and remodels what a cell displays on its surface.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2011 | M | AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1 KIM2011 Second author, supplying the ULK1 loss-of-function background - the kinase's in vivo biology and the Ulk1-null mouse cells - on which the paper's genetic rescue experiments rest. |
Co-authors in the Atlas
People with a profile here who share at least one study with Mondira Kundu.
- Benoit Viollet Showed that metformin still lowers liver glucose production without AMPK or LKB1, pointing instead to a drop in cellular energy charge
- Joungmok Kim Showed as a Guan-lab postdoc that AMPK and mTORC1 control autophagy by phosphorylating ULK1 at different sites, with mTORC1's mark on Ser757 blocking activation by AMPK
- Kun-Liang Guan Showed how growth-factor and energy signals reach mTORC1 through TSC2 and Rheb, and, in parallel with the Sabatini lab, that the Rag GTPases carry the amino-acid signal. His lab also found that AMPK and mTORC1 control autophagy by phosphorylating the kinase ULK1 at different sites
Every researcher with a profile →
On the programme
Meetings in the Atlas calendar where Mondira Kundu is listed among the speakers or organisers.
- upcoming Keystone Symposia: Autophagy in Health and Disease – From Mechanisms to Therapeutics 2027 ↗ 8–11 Feb 2027 · Banff, AB, Canada · ★★