Abstracts - Association for Chemoreception Sciences

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AChemS Association for Chemoreception Sciences Committees AChemS Executive Committee 2009-2010 President Scott Herness, PhD Ohio State University Past President Peter Brunjes, PhD University of Virginia Senior Advisor Diego Restrepo, PhD University of Colorado President Elect Don Wilson, PhD Nathan Kline Institute & NYU School of Medicine Secretary Dana Small, PhD JB Pierce Laboratory/ Yale University Membership Chair Pamela Dalton, PhD Monell Chemical Senses Center Program Chair Robert Margolskee, MD, PhD Monell Chemical Senses Center Treasurer Carol Christensen, PhD Monell Chemical Senses Center Program Chair Elect Matt Wachowiak, PhD Boston University Sr. Councilor Lynette Phillips McCluskey, PhD Medical College of Georgia Jr. Councilor Helen Treloar, PhD Yale University AChemS Program Committee 2009-2010 Robert Margolskee (Chair, 2010) Harriet Baker Frank Margolis Don Wilson Chris Lemon Sue Kinnamon Beverly Tepper Minghong Ma Susan Travers Robin Krimm Paul Moore Hiro Matsunama Noam Sobel Steve Munger Paul Breslin Kazushige Touhara Catherine Rouby Linda Barlow MEETING EVALUATION The meeting evaluation is available online this year. Please visit www.achems.org to give us your feedback on the meeting. Your input helps AChemS’ leadership continue to offer quality annual meetings and member services. 6 | AChemS Abstracts 2010
#1 GIVAUDAN LECTURE Normal and Cancer Stem Cells and the Development of Malignancy Robert A. Weinberg Member, Whitehead Institute and Director, MIT Ludwig Center for Cancer Research The progression of carcinoma cells in primary tumors to a state of high-grade malignancy involves the acquisition of a variety of cell traits, including motility, invasiveness, and an increased resistance to apoptosis. These traits are all components of a complex cellbiological program termed the epithelial-mesenchymal transition (EMT), which normally plays a role in various steps of embryonic morphogenesis and in wound healing. By resurrecting this multifaceted program, cancer cells are able to gain access in a single step to these multiple traits, which in turn empowers them to invade and disseminate. Indeed, the invasive edges of carcinomas often exhibit cells that exhibit signs of having activated an EMT program. Recently it has become apparent that the EMT, rather than creating bona fide mesenchymal cells, actually creates epithelial stem cells that exhibit many mesenchymal traits. Accordingly, the EMT program represents the key to enable the conversion of more differentiated epithelial cells into epithelial stem cells, which holds implications for both normal epithelial cells biology and cancer pathogenesis. #2 PLATFORM PRESENTATIONS - TIP OF THE TONGUE Analysis of Drosophila TRPA1 reveals an ancient origin for human chemical nociception Paul A Garrity 1 , Kyeongjin Kang 1 , Stefan R Pulver 1, 2 , Vincent C Panzano 1 , Leslie C Griffith 1 , Douglas L Theobald 1 1 Brandeis University Waltham, MA, USA, 2 University of Cambridge Cambridge, United Kingdom Chemical nociception, the detection of tissue-damaging chemicals, is important for animal survival and causes human pain and inflammation, but its evolutionary origins are largely unknown. Reactive electrophiles are a class of noxious compounds humans find pungent and irritating, like allyl isothiocyanate (in wasabi) and acrolein (in cigarette smoke). Insects to humans find reactive electrophiles aversive, but whether this reflects conservation of an ancient sensory modality has been unclear. Using a combination of genetics and physiology, we have determined the molecular basis of reactive electrophile detection in flies. We find that dTRPA1, the Drosophila melanogaster ortholog of the human irritant sensor, acts in gustatory chemosensors to inhibit reactive electrophile ingestion. Both fly and mosquito TRPA1 orthologs act as molecular sensors of electrophiles, and they respond to these chemical via a mechanism conserved with vertebrate TRPA1s. Phylogenetic analyses indicate invertebrate and vertebrate TRPA1s share a common ancestor that possessed critical characteristics required for electrophile detection. These findings support emergence of TRPA1-based electrophile detection in a common bilaterian ancestor, with widespread conservation throughout vertebrate and invertebrate evolution. Such conservation contrasts with the evolutionary divergence of canonical olfactory and gustatory receptors and may relate to electrophile toxicity. These findings suggest that human perceptions of reactive electrophiles rely on an ancient chemical sensor conserved across ~500 million years of animal evolution. Acknowledgements: NIMH (R21 MH080206, P.A.G., RO1 MH067284 , L.C.G.) and NINDS (PO1 NS044232) Abstracts are printed as submitted by the author(s) #3 PLATFORM PRESENTATIONS - TIP OF THE TONGUE A subpopulation of mouse Type II taste cells express functional voltage-gated calcium channels Pin Liu, Timothy A. Gilbertson Department of Biology and The Center for Advanced Nutrition, Utah State University Logan, UT, USA Type II taste cells contain receptors and signaling components for sweet, bitter, and umami tastants, and are responsible for transducing complex taste stimuli via the phospholipase C (PLC) pathway. Type II cells communicate with the afferent nerve or Type III cells via non-vesicular purinergic signaling. Previous studies concluded that Type II cells lack voltage-gated Ca 2+ channels (VGCCs), while Type III cells express the VGCCs required for synaptic transmission. However, our functional calcium imaging data in C57Bl/6 mice showed that a small but significant subpopulation of Type II cells, identified by their responses to an established tastant mixture, also responded to high KCl, consistent with the expression of VGCCs in these cells. To explore whether VGCCs are expressed in subpopulations of type II cells, transgenic mice expressing enhanced green fluorescent protein (GFP) under control of the PLCß2 promoter (PLCß2- GFP) were used in both functional calcium imaging and patch clamp recording. Calcium imaging data showed that high KCl elicited a robust intracellular calcium rise in over half of PLCß2- GFP taste cells, consistent with the expression of VGCCs. Patch clamp recording showed that VGCC currents were present in 8 out of 33 PLCß2-GFP taste cells. The VGCC current was large (200~500 pA) when the whole cell configuration was first established, but washed out quickly (t = 138 s). This rapid washout may partially explain why VGCC current has been rarely seen in type II cells electrophysiologically. Our findings strongly suggest that functional VGCCs are expressed in subpopulations of Type II cells and question the current model of cell signaling within the taste bud as well as the utility of high KCl to identify unequivocally type III cells within the taste bud. Acknowledgements: Supported by NIH DK059611 and International Flavors & Fragrances. #4 PLATFORM PRESENTATIONS - TIP OF THE TONGUE Ryanodine Receptors selectively contribute to the formation of Taste evoked-calcium signals in Mouse taste cells Michelle R Rebello, Kathryn F Medler State University of New York at Buffalo Buffalo, NY, USA While it has been well established that different taste stimuli activate distinct signaling pathways in taste receptor cells, the signal transduction mechanisms associated with these pathways have not been completely characterized. Bitter, umami and sweet taste stimuli activate G-protein coupled receptors (GPCRs) to cause Ca 2+ release from intracellular stores, which is known to occur in Type II cells via a PLCb2/IP3R3 signaling pathway. Sour stimuli depolarize taste cells to cause Ca 2+ influx through voltagegated calcium channels (VGCCs), presumably in taste cells with chemical synapses. The transduction pathways of salty stimuli are less well defined. There is also a sub-population of taste cells that express VGCCs and detect bitter taste stimuli but do not express the PLCb2/IP3R3 pathway. These cells are termed dualresponsive and appear to express PLCb3 and IP3R1. While it is recognized that bitter, sweet and umami taste stimuli activate GPCRs to evoke IP3-mediated Ca 2+ release from internal stores, Abstracts | 7
Page 1: AChemS Association for Chemorecepti
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cells within gustatory papillae, we
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excite menthol- and/or CA-sensitive
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gene, HMBS was used. All primers we
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oom, without time keeping devices,
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#P113 POSTER SESSION III: OLFACTORY
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decreasing of endogenous volatiles
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may serve to integrate central and
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esponse magnitudes. Inhibitions rea
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the second a non-specific cation ch
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saline. Some of the labeled ORNs sh
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#P166 POSTER SESSION IV: CHEMOSENSO
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pregnancy block. In order to unders
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of GSP neurons and 97% of PA neuron
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concentrations than flies raised on
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familiarity and cultural difference
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#P265 is found on page 128. #P266 P
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perception of purine 5’-ribonucle
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#P278 POSTER SESSION VI: PERIPHERAL
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(CT), the greater superficial petro
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were significantly different from o
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MSG on NaCl is evidently highlighte
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consisting of motors and IFT comple
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wing. Philip Callahan exposed insec
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seem to indicate that total nasal v
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possibly suggesting non-apoptotic m
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#P325 POSTER SESSION VII: OLFACTORY
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of 7/10, and causing eyes to water
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showed that N1/P2 latencies were lo
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differentiated patients with AD (M=
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pleasantness 3)of mixtures (A,B), A
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Index Aarts, H - P328 Abe, K - P88,
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Haase, L - P3, P4, P29, P355 Haddad
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Murata, Y - P272 Murphy, C - P3, P4
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Veldhuizen, M - P7, P24, P25, P242,
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Registration 7:30 am to 1:00 pm, 6:
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See you next year! AChemS 33rd Annu
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Abstracts - Association for Chemoreception Sciences

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