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) ↗

Mondira Kundu 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

A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.

Year	Evidence	Study
2010	M	Phosphorylation of ULK1 (hATG1) by AMP-activated protein kinase connects energy sensing to mitophagy EGA2010 AMPK directly phosphorylates ULK1 to connect energy sensing to autophagy/mitophagy, opposing mTOR.
2011	M	Ulk1-mediated phosphorylation of AMPK constitutes a negative regulatory feedback loop LOF2011 ULK1 phosphorylates and inhibits AMPK in return, showing autophagy signaling is a bidirectional feedback loop, not a one-way switch.
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 13

People with a profile here who share at least one study with Mondira Kundu.

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Benoit Viollet 2 shared studies Showed that metformin still lowers liver glucose production without AMPK or LKB1, pointing instead to a drop in cellular energy charge
Antje S. Löffler Cell biologist who worked in Björn Stork's group on how the autophagy kinase ULK1 talks back to the energy sensor AMPK
Björn Stork Heisenberg Professor for the molecular biology of cellular stress responses at Heinrich Heine University Düsseldorf, who studies the ULK1 complex, the switch that starts autophagy, and how it is wired to the energy sensor AMPK and to mTOR
Dana M. Gwinn First author of the 2008 study showing that the energy sensor AMPK switches off mTORC1 by phosphorylating raptor
Daniel F. Egan Showed as first author that AMPK directly phosphorylates ULK1, linking low cellular energy to autophagy and mitophagy, and contributed to the finding that AMPK brakes mTORC1 by phosphorylating raptor
Dario R. Alessi Co-discovered PDK1, the master kinase that switches on Akt and related AGC kinases, and showed that mTORC2 activates the kinase SGK1
David B. Shackelford Cancer biologist at UCLA who studies lung tumours that have lost the LKB1 tumour suppressor, the upstream activator of AMPK, and who trained in Reuben Shaw's lab at the Salk Institute
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.
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
Malene Hansen Showed in worms, alongside a 2007 report from Beth Levine's laboratory, that autophagy is required for dietary restriction to extend lifespan
Maria M. Mihaylova Studies how intestinal stem cells change with age and how diet shapes their metabolism
Reuben J. Shaw Showed, in parallel with two other groups, that the tumour suppressor LKB1 directly activates AMPK, and that AMPK brakes mTORC1 by phosphorylating raptor. His Salk lab also linked AMPK to autophagy through ULK1 and helped explain how metformin acts in the liver

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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 · ★★ Add to calendar: Google · Apple / Outlook

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