ECS Fellows 2014

ECS 2014 FELLOWS
Bipan Kumar Deb National Centre for Biological ScienceswTata Institute of Fundamental ResearchwBangalorewIndia My work in Prof. Gaiti Hasan’s laboratory is aimed at understanding the function of septins in regulation of neuronal Ca2+ signaling and store-­‐operated Ca2+ entry (SOCE) in Drosophila. Our lab studies the role of IP3 receptor stimulated Ca2+ signaling and SOCE in the context of development and functioning of the flight circuit in the fruit fly. A recent report (Sharma et al, Nature, 2013) had shown a critical role for septin dynamics in organization of the CRAC channel, Orai in HeLa and Jurkat T cells. I am interested in understanding if this regulatory role for septins is conserved in neurons and if so, whether it affects neuronal function and flight behavior. Preliminary investigations unraveled a genetic interaction of the Drosophila septin Pnut with IP3 receptor, STIM and Orai in the flight circuit. This motivated me to investigate the effect of modulating the levels of Pnut on neuronal Ca2+ homeostasis. I am currently recording the nature and dynamics of calcium homeostasis from primary neuronal cultures derived from animals with or without a genetic perturbation of Pnut function. I am using this information obtained at a single cell level to understand and explain how this regulation of the neuronal Ca2+ homeostasis by this filament forming GTPase finally affects a complex motor coordination behavior like flight in the adult fly. Interestingly, my work shows that the modulatory role for Pnut in neuronal SOCE is distinct from what has been described earlier for mammalian septins, SEPT2, 4 and 5 in HeLa and Jurkat T cells. This is particularly exciting as it hints at a possibility for a differential role for different septins in regulation of neuronal calcium homeostasis. I am also using cellular imaging techniques to decipher the molecular mechanisms involved in this process. Presentation of my work at the ECS meeting 2014 will help me get critical reviews from eminent scientists and fellow research scholars working in the field of Ca2+ signaling. It will also provide me a platform to meet a number of renowned scientists, from whom I can seek advice on several aspects of my ongoing and future research work. Moreover, I would get an opportunity to gather knowledge about the several exciting and ongoing advances in the field of calcium signaling. This in turn would help shape my understanding of the calcium research field and review the significance of my findings in the broader context of this field. ABSTRACT TITLE Drosophila septin, Pnut is a modulator of neuronal Store operated calcium entry 1 Ellen Gattkowski Department of Biochemistry and Molecular Cell Biology wUniversity Medical Centre in Hamburg-­‐Eppendorf wGermany I am in Prof. Guse’s lab since the beginning of 2014 to complete my bachelor thesis. The main interests of the group are second messenger-­‐mediated Ca2+signaling in various cell types. My thesis deals with the analysis of elementary Ca2+ signals evoked by NAADP upon microinjection. I decided to work in the Calcium field and join the ECS because Ca2+ signaling is a fundamental signaling pathway of great importance in various biochemical processes which is nonetheless not yet fully understood. I’m looking forward to attend the ECS meeting and gain insights into actual findings of various topics concerning the wide calcium field. The meeting of the ECS in Aix-­‐en-­‐Provence is the first opportunity for me to present and discuss my own research results. Moreover, attending this meeting I get the unique chance to listen and meet internationally recognized scientists working in the Calcium field. ABSTRACT TITLE Analysis of elementary Ca2+ signals in T-­‐Lymphocytes evoked by microinjection of NAADP Gaia Gherardi Dept. of Biomedical Sciences w University of Padua wI taly 2 I am a PhD student of the University of Padua (Italy) and I work in the laboratory of Professor Rosario Rizzuto, under the supervision of Doctor Cristina Mammucari. The research of our group is focused on the study of mitochondrial calcium uptake pathway. In 2011 our group discovered the molecular identity of the mitochondrial calcium uniporter (MCU). My PhD project investigates the pathophysiological role of mitochondrial Ca2+ uptake and oxidative metabolism in the control of skeletal muscle homeostasis. Loss of muscle mass and performance occur during pathological conditions like disuse, denervation, starvation and cancer and contribute to the worsening of life expectancy. In addition, muscle atrophy accompanies aging. Therapeutic strategies aimed to preserve muscle mass are of key importance, but they are still limited. The aim of the project is to investigate whether novel therapies can by envisioned by modulating mitochondrial Ca2+ signalling. The ECS symposium is for me an opportunity to meet and discuss new ideas with established scientists and students, in order to improve the future perspectives of this project. ABSTRACT TITLE The role of the Mitochondrial Calcium Uniporter in the control of skeletal muscle mass. Melissa Magnusson Åbo Akademi UniversitywBioscienceswTurkuwFinland During my M. Sci I started working with calcium signaling in cancer research under the supervision of Professor Kid Törnquist. During this project I developed an interest in calcium channels and I decided to follow my interests by applying for a PhD position within the same research group. I started my PhD in May 2014. My project focuses on the TRPC1 cation channel in ML-­‐1 thyroid cancer cells. Calcium is a crucial regulator of migration and recently TRPC channels have been implicated in cancer cell migration and metastasis. However, few studies have investigated the role of these channels in regulating migration and proliferation of thyroid cancer cells. Thus, the aim of my project has been to characterize the TRPC1 cation channel in ML-­‐1 thyroid cancer cells and examine its role in regulating migration and proliferation of these cells. I am very excited to have gotten the opportunity to attend this conference and to interact with leaders in this field at such an early point in my career. Attending this conference will certainly give me a great opportunity to broaden my insights in the complex field of calcium research. Finally, I have no doubt that this conference will be of great value for my future development as a young scientist. TITLE ABSTRACT TRPC1 channel knock-­‐down attenuates the expression of receptors involved in migration of ML-­‐1 cells 3 Valerio Marino Department of Life Sciences and ReproductionwSection of Biological Chemistry wUniversity of VeronawItaly During the first year as a graduate student at Dr. Dell’Orco’s lab I have been working on different projects concerning biophysical and structural properties of Neuronal Calcium Sensors involved in phototransduction and their interaction with CaF2 nanoparticles. I also had the opportunity to visit Prof. Koch’s lab to get expertise on molecular biology and biochemical techniques useful to study specific calcium sensors operating in the phototransduction cascade. The 2014 ECS meeting will provide me with an unique chance to share my recent findings about the role of Mg2+ in the regulatory states of Recoverin, GCAP1 and GCAP2 with colleagues from all around the world and renowned scientists who will hopefully help me shedding light on some unclear aspects of the topic or pitch ideas on possible future developments. This will also be my first international meeting and I am really looking forward to gathering a more comprehensive picture of the various roles that Ca2+ plays in the regulation of different biochemical processes. ABSTRACT TITLE Structural effects of Mg2+ on the regulatory states of Neuronal Calcium Sensors operating in vertebrate phototransduction 4 JongYun Myeong Department of physiologywSeoul national university college of medicinewRepublic of Korea My current project in Prof. So’s lab is to investigate the mechanism and regulation of transient receptor potential channel. My work majorly focuses on the regulation of activation in the transient receptor potential cation (TRPC) 1/4/5channel. TRPC channel is the Ca2+-­‐permeable nonselective cation channel that is activated by wide variety of stimuli. Functional TRPC channel consists of homo or hetero tetrameric structure, and are expressed in many tissues such as brain, retina, and substantia nigra. I found that N-­‐terminal of TRPC4/5 channel has the membrane targeting domain. Our lab recently found that Gαi is the main activation protein for TRPC4/5 channels. Malfunction of these channels cause a number of diseases by either an increase or decrease of Ca2+ since TRPC1/4/5 are Ca2+ permeable channels. Currently, my study is about transient receptor potential polycystic (TRPP1/2) which is known to play a major role in the cause polycystic kidney diseases when they have mutations. TRPP channels are thought to be located in primary cilia of cells. TRPP and cilia are considered to mediate calcium signal from cilia to the body of cell. My presentation in the 2014 ECS meeting will navigate me to pave a new way about research in unexplored field in TRPP channel and the primary cilia. Abstract title Identification of Membrane Targeting Domain of Transient Receptor Potential Canonical (TRPC)4 Channel unrelated to its Formation of Tetrameric Structure 5 Iulia Nita Department of Physiology and Cell BiologywFaculty of Health ScienceswBen Gurion UniversitywIsrael I am PostDoc, working with Prof. Israel Sekler. My research project is focused on investigation of crosstalk between plasma membrane Ca2+ and Na+ channels and mitochondrial Ca2+ transporters (uniporter and mitochondrial Na+/Ca2+ exchanger) in pancreatic β cells. Previously, we showed that the mitochondrial Ca2+ shuttling via mitochondrial Na+/Ca2+ exchanger modulates glucose dependent Ca2+ signaling and temporal pattern of insulin secretion (see Nita I.I. et al. Plos One, 7(10): 1-­‐10, 2012) Mitochondrial Na+/Ca2+ exchanger mediates Ca2+ efflux in a Na+ dependent manner and further, we continued our investigations on crosstalk between voltage gated Na+ channels and mitochondrial Ca2+ shuttling via mitochondrial Na+/Ca2+ exchanger. Our results showed that Na+ channels provide Na+ substrate for activation of mitochondrial Na+/Ca2+ exchanger, controlling the duration of mitochondrial Ca2+ transients and thus, modulating the rate of glucose dependent cytosolic Ca2+ rise and insulin secretion. In addition, voltage gated Na+ channels enhances the glucose dependent cytosolic Ca2+ rise by further depolarization of cell membrane, followed by an increase in rate of mitochondrial Ca2+ influx and subsequently, accelerated oxidative metabolism. Recently, some of the results were published in the article: Nita I.I. et al. FASEB Journal, 28(8): 3301-­‐12, 2014. Attending 13th International Meeting of the European Calcium Society, I will have the opportunity to learn and to interact with leaders in the field, while I will present the novel and significant role of Na+ channels in regulation of global Ca2+ signalling and metabolism in pancreatic β cells. ABSTRACT TITLE Functional interplay between Na+ channels and mitochondrial Ca2+ transporters controls the global Ca2+ dynamics and oxidative metabolism in pancreatic β Cells 6 Meerim Nurbaeva New York UniversitywCollege of DentistrywDepartment of Basic Science and Craniofacial BiologywNew YorkwUSA The research interest of our group is to investigate the mechanisms regulating intracellular Ca2+
concentration in epithelially-derived enamel forming cells. These cells, termed ameloblasts, regulate
the complex process of enamel development and mineralization. Although Ca2+ is a key element in the
composition of dental enamel, the mechanisms used by ameloblasts to actively transport Ca2+ remain
poorly understood. Our unpublished data show that CRAC (Ca2+ release activated Ca2+) channels likely
mediate Ca2+ uptake in ameloblasts. These novel data may help explain the deficiencies in enamel
development in patients with mutations to CRAC associated proteins STIM and ORAI.
Having the possibility of presenting our work at European Calcium Society (ECS) meeting is a unique
opportunity to exchange ideas, seek suggestions and to gather constructive criticisms. The ECS
meetings are especially relevant to my professional expertise because of my keen interest in
understanding all aspects related to Ca2+. I am really looking forward to this event attended by experts
from all over the world. The conference features an excellent pool of keynote speakers, podium
presentations and posters. Learning from all of these experiences will greatly benefit my own work.
ABSTRACT TITLE A Novel Mechanism for Ca2+ Uptake by Enamel Forming Cells 7 Gustavo Pereira Federal University of Sao PauloPharmacology DepartmentBrazil I am PhD student working under the supervision of Dr. Soraya Smaili on Apoptosis and Autophagy in Neurodegeratives Diseases and relationship with Ca2+ Signalling. My main work is based about the Nicotinic acid adenine dinucleotide phosphate (NAADP) that is a potent Ca2+ mobilizing messenger that in many cells releases Ca2+ from the endo-­‐lysosomal system. Recently study published for us suggest that its Ca2+ mobilizing effects are mediated by the two-­‐pore channels (TPCs), specially TPC type 2 and this signalling might to participate in the regulation of autophagy. Nowadays, I am investigating the mechanism of action of NAADP in autophagy pathways in colaboration with Dr. Sandip Patel from University College London, London, UK, and Dr. Mauro Piacentini e Dr. Gian Maria Fimia, from National Institute for Infectious Diseases IRCCS 'Lazzaro Spallanzani', Rome, Italy. For this purpose, this congress would be an excellent opportunity to learn more about Ca2+ signaling, cell death and autophagy mechanisms and discuss about my work and to know about some works that will be presented. I also consider that it will be a major opportunity to meet researchers in the area who share the same interests. ABSTRACT TITLE 2+
NAADP mediated Ca Signaling and Regulates Autophagy Glutamate-­‐induced in Astrocytes 8 Maria Ryazantseva Laboratory of ionic channels of cell membraneswInstitute of Cytology RASw St. PetersburgwRussia My PhD project is devoted to study of calcium signaling in neurons impaired in familial Alzheimer’s disease connected with mutations in presenilin-­‐1 gene. Our group found store-­‐operated calcium channels to be involved in pathological mechanism of memory loss in Drosophila m. Alzheimer’s disease model. The ECS 2014 meeting is great opportunity to present my new data and meet professional opinion and criticism. Moreover I interested in calcium signaling per se and the meeting is the best way to get new knowledge in this broad field: from new molecular players to new approaches. I believe that the meeting will inspire me for future studies and improve my development as young researcher. ABSTRACT TITLE STIM sensors as molecular targets for memory loss treatment connected with calcium homeostasis impairments in Familial Alzheimer’s Disease Karolina Varga Institute of EnzymologywResearch Centre for Natural ScienceswHungarian Academy of ScienceswBudapestwHungary 9 I started my PhD program in September 2010 in the Calcium Transport Laboratory, supervised by Dr. Ágnes Enyedi at the Institute of Enzymology, Hungarian Academy of Sciences. Our group investigates the structure, function, expression and localization of the plasma membrane calcium ATPases. In my PhD project I focus on the question of how these characteristics of these pumps change during breast cancer cell differentiation induced by histone deacetylase inhibitors. An article based on my results in MCF-­‐7 cells has been published in Cell Calcium in February 2014. At present I am working further on this topic to extend our knowledge to other breast cancer cell lines, and to understand how PMCAs are regulated in breast cancer cells treated with several epigenetic drugs. I attended the previous ECS Meeting in Toulouse two years ago, and I found it very useful. I heard excellent lectures and I had great opportunity to discuss my results with some excellent researchers from the field of calcium signaling that was especially helpful during the preparation of my article. I would like to present some of our recent results on the 13th ECS Meeting in Aix-­‐en-­‐Provence. I will certainly benefit from the forthcoming conference especially because this year a whole session is dedicated to my current research topic: Ca2+-­‐channels and pumps and cancer. ABSTRACT TITLE Differential effects of histone deacetylase inhibitors on the expression of PMCAs in breast tumor cells Tamara Vervloessem KU LeuvenwCellular and Molecular MedicinewLeuvenwBelgium Participating in the international meeting of the European calcium society will give me the chance to share the results that I have obtained so far during my research with colleagues. Likewise, I have already had the opportunity to present my data at the Belgian Association for Cancer Research earlier this year, which I found a very interesting and positive experience. My PhD-­‐study focuses on the effect of anti-­‐apoptotic Bcl-­‐2 at the level of the endoplasmic reticulum, the main intracellular calcium store. Moreover, we try to scrutinize the fundamental working mechanism of Bcl-­‐2 and also to exploit these properties to selectively elicit “toxic” calcium signals in B-­‐cell cancer. Additionally, preliminary data look very promising and therefor it will be useful, while attending the congress, to exchange ideas for my work with experts in the field and to learn from their experience. Furthermore, as the main focus of my research is lying on the IP3-­‐induced calcium signaling in B-­‐cell cancers (diffuse large B-­‐cell lymphoma and chronic lymphocytic leukemia), I’m especially looking forward to the presentation of for example Jacques Haiech and Martin Falcke, who will give a general overview of calcium signaling in cancer stem cells and the general properties of IP3-­‐induced calcium spiking respectively. I see this meeting as an opportunity to also gather inspiration for experiments and the further progression of my PhD. I really look forward to improve my calcium-­‐specific knowledge as I would 10 like to play a key-­‐role in my laboratory, which is specialized in calcium-­‐signaling. Moreover, I am hoping to further develop myself by attending the meeting, so that I can make an important contribution in the domain of calcium through my research. ABSTRACT TITLE Transforming pro-­‐survival IP3 signaling in B-­‐cell cancers into pro-­‐apoptotic Ca2+ signaling upon Bcl-­‐2 antagonism at the endoplasmic reticulum Kunsala Yapa The University of QueenslandwSchool of PharmacywBrisbanewAustralia ` I work in the calcium signalling in cancer research laboratory under the supervision of Professor Greg Monteith and Professor Sarah Roberts-­‐Thomson. My PhD project focuses on the study of calcium channels and pumps involved in the proliferation and migration of breast cancer cells. Many studies have shown that aberrant expression of specific calcium pumps and channels is a feature of some breast tumours. The aim of my research is to identify and characterise calcium transporters involved in breast cancer pathogenesis. I am in the second year of my PhD and it has been a very rewarding experience thus far. The skills and knowledge I have gained from my PhD has ignited my interest in the calcium signalling field and I believe attending this conference will be a valuable experience and further my education in calcium research. This meeting is a rare opportunity to meet the foremost experts in the calcium signalling field and I think it will be extremely beneficial for my future research career. ABSTRACT TITLE Effect of ATMB, a pharmacological modulator of TRPM8 on breast cancer cell proliferation 11