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Hai-Ying Mary Cheng
Assistant Professor
Department of Biochemistry, Microbiology and Immunology
Faculty of Medicine, University of Ottawa

Roger Guindon Hall, Room 4173 (office) and Room 2223 (lab)
451 Smyth Road, Ottawa, ON K1H 8M5

Tel: 613-562-5800 ext. 8908 (office)
Tel: 613-562-5800 ext. 8497 (lab)

Email: mchen2@uottawa.ca

We currently have the following opportunities see jobs section.


Hai-Ying Mary Cheng
Assistant Professor

Degrees:

B.Sc. (hons) University of Calgary, 1996
M.Sc. University of Toronto, 1999
Ph.D. University of Toronto, 2003
Post-doctoral fellow, University of Toronto and The Ohio State University, 2003-2007

Research Projects

All organisms have biological clocks, which drive and coordinate circadian rhythms in behaviour and physiology in accordance with the demands of our 24-hour world. In mammals, the master biological clock resides in the suprachiasmatic nuclei (SCN) of the hypothalamus. The SCN has endogenous pacemaker activity that runs at near-24-hour cycles and is regulated by the environmental light cycle, thereby allowing the organism to synchronize its internal clock timing mechanism with daily and seasonal variations in the day/night cycle. Many of us are familiar with the adverse effects of a disrupted biological clock—as a result of environmental conditions (eg., jet lag, night-shift work), or , for the more unfortunate, genetic inheritance (eg., familial advanced sleep phase disorder) and disease (eg., cancer, bipolar disorder). While genetic studies have established that the circadian clock is comprised of a set of ‘core’ clock proteins that interact in interlocking transcription/translation feedback loops to drive rhythms in their own gene expression, our knowledge of the regulatory processes that feed into this molecular clock remains nebulous. Which cascades of cellular events are needed to couple environmental light to the molecular clock? How do individual clock cells synchronize with each other to produce an ensemble rhythm in a tissue? How does aberrant regulation of the circadian clock impact on other biological clocks such as the one controlling cell division? The overall objective of our laboratory is to elucidate the cellular mechanisms that regulate biological timing in mammals, and, in turn, to understand how these cellular mechanisms manifest themselves at the “organism” scale such as animal behaviour, and play a role in diseases arising from their abnormal functioning.

Selected Publications:

  1. Cheng HYM, Obrietan K. (2008). The mammalian circadian clock: signal transduction pathways and transcriptional regulation. In Transcriptional Regulation by Neuronal Activity: To the Nucleus and Back, S.M. Dudek, ed. (New York, Springer), pp. 313-336.
  2. Cheng HY, Obrietan K. (2007). Revealing a role of microRNAs in the regulation of the biological clock. Cell Cycle. 6(24):3034-3038.
  3. Cheng HYM, Papp JW, Varlamova O, Dziema H, Russell B, Curfman JP, Nakazawa T, Shimizu K, Okamura H, Impey S, Obrietan K. (2007). MicroRNA modulation of circadian clock period and entrainment. Neuron. 54(5):813-829.
  4. Huang H, Acuna-Goycolea C, Li Y, Cheng HM, Obrietan K, van den Pol AN. (2007). Cannabinoids excite hypothalamic melanin-concentrating hormone but inhibit hypocretin/orexin neurons—implications for cannabinoid actions on food intake and cognitive arousal. J Neurosci. 27(18):4870-4881.
  5. Cheng HYM, Dziema H, Papp J, Mathur DP, Koletar M, Ralph MR, Penninger JM, Obrietan K. (2006). The molecular gatekeeper Dexras1 sculpts the photic responsiveness of the mammalian circadian clock. J Neurosci. 26(50):12984-95.
  6. Cheng HYM, Obrietan K. (2006). Dexras1: shaping the responsiveness of the circadian clock. Semin Cell Dev Biol. 17(3):345-51.
  7. Butcher GQ, Lee B, Cheng HY, Obrietan K. (2005). Light stimulates MSK1 activation in the suprachiasmatic nucleus via a PACAP-ERK/MAP kinase-dependent mechanism. J Neurosci. 25(22):5305-13.
  8. Cheng HYM, Obrietan K, Cain SW, Lee BY, Agostino PV, Joza NA, Harrington ME, Ralph MR, Penninger JM. (2004). Dexras1 potentiates photic and suppresses non-photic responses of the circadian clock. Neuron. 43(5):715-28.
  9. Cheng HYM, Laviolette SR, van der Kooy D, Penninger JM. (2004). DREAM ablation selectively alters THC place aversion and analgesia but leaves intact the motivational and analgesic effects of morphine. Eur J Neurosci. 19(11):3033-41.
  10. Wada T, Joza N, Cheng HY, Sasaki T, Kozieradzki I, Bachmaier K, Katada T, Schreiber M, Wagner EF, Nishina H, Penninger JM. (2004). MKK7 couples stress signalling to G2/M cell-cycle progression and cellular senescence. Nat Cell Biol. 6(3):215-26.
  11. Crackower MA, Oudit GY, Kozieradzki I, Sarao R, Sun H, Sasaki T, Hirsch E, Suzuki A, Shioi T, Irie-Sasaki J, Sah R, Cheng HY, Rybin VO, Lembo G, Fratta L, Oliveira-dos-Santos AJ, Benovic JL, Kahn CR, Izumo S, Steinberg SF, Wymann MP, Backx PH, Penninger JM. (2002). Regulation of myocardial contractility and cell size by distinct PI3K-PTEN signaling pathways. Cell. 110(6):737-49.
  12. Cheng HY, Pitcher GM, Laviolette SR, Whishaw IQ, Tong KI, Kockeritz LK, Wada T, Joza NA, Crackower M, Goncalves J, Sarosi I, Woodgett JR, Oliveira-dos-Santos AJ, Ikura M, van der Kooy D, Salter MW, Penninger JM. (2002). DREAM is a critical transcriptional repressor for pain modulation. Cell. 108(1):31-43.
  13. Osawa M, Tong KI, Lilliehook C, Wasco W, Buxbaum JD, Cheng HY, Penninger JM, Ikura M, Ames JB. (2001). Calcium-regulated DNA binding and oligomerization of the neuronal calcium-sensing protein, calsenilin/DREAM/KChIP3. J Biol Chem. 276(44):41005-13.
  14. Joza N, Susin SA, Daugas E, Stanford WL, Cho SK, Li CY, Sasaki T, Elia AJ, Cheng HY, Ravagnan L, Ferri KF, Zamzami N, Wakeham A, Hakem R, Yoshida H, Kong YY, Mak TW, Zuniga-Pflucker JC, Kroemer G, Penninger JM. (2001). Essential role of the mitochondrial apoptosis-inducing factor in programmed cell death. Nature. 410(6828):549-54.
  15. Irie-Sasaki J, Sasaki T, Matsumoto W, Opavsky A, Cheng M, Welstead G, Griffiths E, Krawczyk C, Richardson CD, Aitken K, Iscove N, Koretzky G, Johnson P, Liu P, Rothstein DM, Penninger JM. (2001). CD45 is a JAK phosphatase and negatively regulates cytokine receptor signalling. Nature. 409(6818):349-54.