Greg Suh, PhD

Associate Professor; Skirball Institute of Biomolecular Medicine, Molecular Neurobiology. Department of Cell Biology

Suh Lab

Cell Biology, Skirball Institute of Biomolecular Medicine




Contact Information

540 First Avenue
Skirball Institute of Biomolecular Medicine
Floor 5, Lab 13
New York, NY 10016

Office Tel: (212) 263-3024
Tel: (212) 263-5975
Fax: (212) 263-8214 Email:

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Dolly Chan
Tel: (646) 501-0679

Gene and Neural Circuit mediating Innate Behavior

Acid Receptor in the Drosophila olfactory system
The acid odor has a distinct quality that is perceived as sharp, pungent and often irritating. How acidity is sensed and translated into an appropriate behavioral response is poorly understood. Our laboratory described a functionally segregated population of olfactory sensory neurons (OSNs) in the fruit fly, Drosophila melanogaster, that are highly selective for acidity. These OSNs express IR64a, a member of the recently identified Ionotropic Receptor (IR) family of putative olfactory receptors. In vivo calcium imaging showed that IR64a+ neurons projecting to the DC4 glomerulus in the antennal lobe are specifically activated by acids. Flies in which the function of IR64a+ neurons or the IR64a gene is disrupted had defects in acid-evoked physiological and behavioral responses, but their responses to non-acidic odorants remained unaffected. Furthermore, artificial stimulation of IR64a+ neurons elicited avoidance responses. Together, these results identify cellular and molecular substrates for acid detection in the Drosophila olfactory system and support a labeled-line mode of acidity coding at the periphery.

Taste-independent Sugar Sensor in the brain
Feeding is influenced by multiple factors such as nutritional needs and food palatability. Peripheral chemosensory neurons such as sugar receptor neurons endow animals to detect palatable food. Additional mechanisms would exist for the detection of foods that meet nutrient needs. Indeed, our laboratory showed that the Drosophila mutants- GR5a;GR64a and pox-neuro mutants- that are insensitive to the taste of sugar still developed a preference for a sugar solution based on its nutritional value after prolonged periods of food deprivation. Specifically, these starved sugar-blind or taste-blind flies were able to distinguish nutritious D-glucose from zero-calorie L-glucose, which tastes almost identical as D-glucose to flies. These findings suggest that there exists a taste-independent sensor that detects its caloric content. Using two-choice preference assay (D-glucose versus L-glucose), we carried out a small-scale screen for an internal sugar sensor and identified a mutation in a Sodium/Glucose co-transporter, dSGLT11, that was completely insensitive to the caloric content of sugar, but rather responded only to the concentration of sugar- “sweetness”. Surprisingly, dSGLT11 is expressed in 10 pairs of neurons in the brain. We are currently characterizing the function of dSGLT11 gene and dSGL11+ neurons. These studies will not only fundamentally transform our understanding of chemosensory biology, but will also provide a valuable framework for understanding the mechanisms by which appetite is regulated by metabolic needs in normal, and obese patients.