ContentsContents

EditorialEditorial

Editorial (M. Moreau & C. Leclerc) p1

Meeting reports p2

Highlights of the meeting p14

ECS workshops p15

Announcements p16

To your agenda p18

New board p19

The president of the ECs writes

(Marc Moreau)

p20

This issue of the ECS newsletter

is mainly devoted to the reports of the

last ECS meeting held in Toulouse in

last September. There was a friendly

atmosphere, very good scientific discus-

sions and an important participation of

junior researchers.

The poster sessions were very

busy, may be the open beer bar was for

something in this success!

Next year in few months (time is

running fast) two ECS workshops will

be organized and it is time to think

about the program of the next meeting

in 2014. A scientific board will be done

at the beginning of 2013 and will be

presented in the next issue of the news-

letter.

The size of this newsletter is in-creasing, this is important for the visibil-ity of our Society. As it was written be-fore we want to have a real journal, with history, scientific articles or opinions, debates, announcements etc... Try to propose spontaneously articles.

Marc Moreau & Catherine Leclerc

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Editorial staff: catherine Leclerc & marc Moreau

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The 12th ECS meeting was organ-ized in Toulouse and was for the first time opened by a plenary lecture given by a scientist working in plant biology. Such lectures are usually given by scientists work-ing on animal models that represent the vast majority of participants attending the ECS meeting. Another novelty of this meeting was to include in each session a lecture from sci-entists coming from the plant Ca2+ signaling field. Thus we could have lectures from Tina Romeis (Department of Biology, Biochemistry and Pharmacy of Berlin -Germany), Hillel Fromm (Department of Molecular Biology and Ecology of Plants in Tel-Aviv -Israel) and David Barker (Laboratory of Plant-Microbe Interactions in Castanet -Tolosan -France).

As already underlined, the plenary lecture was given by Pr. Jorg Kudla, a European leader in plant Ca2+ signaling work-ing at the Institute of Plant Biology and Bio-technology at the University of Munster (Germany). His lecture illustrated how most of the questions arising in plant Ca2+ signaling can be similar to those risen in animal field and how they can be answered using the most up-to-date approaches. Thus, after an introduction about the decoding Ca2+ toolkit in plants, J. Kudla, focused on his favorite model i.e. the plant specific Ca2+ sensors family of CBL (for Calcineurin-B-like) and their downstream targets (referred as to CIPKs for CBL interacting protein kinases). Pointing the fact that plant calcineurin-B-like are associ-ated to a kinase activity and not to a phos-phatase activity as shown in animals, he illus-trated how this model can be useful to reveal the complexity of the signaling network cre-ated by the selective and conditional interac-

tions that can occur between CBLs and their targets. He stressed out the amenability of this model to address the question of how specificity could be achieved with Ca2+ signa-tures and how the relative stoichiometry and/or post-translational modifications (myristoylation and palmitoylation) of partners at one time and in a single cell can orientate the signaling pathway towards a specific re-sponse. Indeed a specific targeting and/or localization of CBL/CIPK complexes contrib-ute to regulate the activity of potassium or anionic channels, ROS production, light re-sponse…. Jörg Kudla showed through the work performed in his group how the most up-to-date techniques such as electrophysiology, TIRF, Ca2+ imaging with Cameleon-Ca2+ probes, protein–protein interaction using BiFc and site-directed mutagenesis can be judi-ciously combined to decipher molecular mechanisms involved in Ca2+ signaling in plants.

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Plenary Lecture/

Pr Jorg Kudla by Christian Mazars

Report on the 12th ECS Meeting: Toulouse 2012 (September 9-12)

Prof. Dr. Jörg Kudla

After Chikashi Toyoshima and Katsu-hiko Mikoshiba, Anjana Rao from the La Jolla Institute of Allergy and Immunology in Califor-nia, USA, was the 3rd recipient to be awarded with the Michael Berridge lectureship to be delivered at the 12th meeting of the European Calcium Society in Toulouse. Since many years Dr. Rao is one of the leading experts in the field of Ca2+ signal-ing, especially of the immune system. In an excellent overview she summarized the inter-play of some of the important factors respon-sible for Ca2+ signaling. Sustained Ca2+ entry is critical for most responses of the different cells of the immune system. In 1986 Putney suggested that depletion of the Ca2+ stores of the endoplasmic reticulum could evoke sus-tained Ca2+ influx through the plasma mem-brane, the so-called store operated Ca2+ entry (SOCE). However, the molecular identities of the two key players involved in the regulation of Ca2+ entry through Ca2+ release-activated Ca2+ or CRAC channels, ORAI and STIM, have been identified about 20 years later through extensive RNAi screens, mainly by the labs of Anjana Rao and Tobias Meyer, respectively. ORAI, a four transmembrane domain containing protein, is located in the plasma membrane; it turned out to represent the CRAC channel. Dr. Rao also described a number of loss-of-function mutations of ORAI1 which resulted in a severe T cell immune deficiency. ORAI is gated by STIM, the EF-hand contain-ing Ca2+ sensor located in the ER. One of the consequences of Ca2+ entry due to the stimu-lation of the cell is the dephosphorylation of NFAT, the Ca2+-regulated transcription factor, via the calmodulin-dependent phosphatase calcineurin. This enables NFAT to translocate to the nucleus which is essential for effective

transcriptional activity. After the detailed de-scription of the general machinery involved in Ca2+ signaling to gene transcription through store-operated Ca2+ entry via ORAI, STIM and NFAT Dr. Rao described in a stimulating way a number of unpublished data in which she and her co-workers attempted to identify further modulators of this complex signaling system. Dr. Rao provided evidence that some specific septins are involved in the membrane organization of ORAI influencing the interac-tion with STIM to regulate Ca2+ entry. These septins seem to be different from those in-volved in cytokinesis. It was fascinating to hear that in septin depleted cells ORAI clus-tering within the plasma membrane and the rate and extent of STIM to move to the plasma membrane to regulate ORAI action was significantly impaired. Similarly, septin depletion also inhibited the nuclear transloca-tion of NFAT. This stimulating lecture by Dr. Rao shed light on the high complexity of this Ca2+-signaling pathway regulated through store-operated Ca2+ entry.

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Plenary Lecture/

Dr. Anjana Rao by Joachim Krebs

Dr. Anjano Rao

Calcium Binding proteins (CaBP) be-cause of their names, needs to bind Ca2+ and only Ca2+. Nature is sometimes willing to use pliers instead of a hammer. For a dogmatic scientist, Nature is annoying. Always some-thing is over. CaBPs bind everything, namely mag-nesium, potassium, sodium, zinc,…, probably

anything existing in the cytoplasm even water molecule. What the hell to call those proteins CaBPs? Ca2+ is the messenger that has to be decoded. Anything else is a modulator. Therefore, what you see in your test tube is not what will happen in the cell, as it is impos-sible to record everything in the cell. And the challenge is to link the real quantitative world of the biophysicist (with as few parameters as

possible) with the esthetic and fashionable feelings of the cell biologists, not speaking about the physiologists. How to link mathe-matical models and a tale? How to reconcile science and arts? It is this unreachable aim that we pur-sue in the ECS meetings. On top of that, we try to present in the same exhibition “green

art” and “animal style art”, as hard as to fuse

Picasso and Lascaux Tags, but it is working. The first session was trying to sort out this incredible mess. This is illustrated the above map.

Beat Schwaller in the keynote lecture reminds us that CaBPs are not only Ca2+ sen-sors but also modulates the shape of the Ca2+ signature. Then, went the green part of the session with the talk of Hillel Fromm, showing

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Session/

CaBP target & Inhibitor by Jacques Haiech

that plant scientists may bring new ideas and fresh air to the field. As we knew that the Nobel Prize will

be awarded to GPCR topics, Daniella Ric-cardi told us about the only GPCR that is also a Ca2+ sensor. As usual when you speak “calcium”, this protein was realizing a lot of

functions depending of the context.

Madeline Shea convinced us that Na-ture is reusing over and over the same tricks. Calmodulin is a haemoglobin-like protein that binds Ca2+ instead of oxygen. But, Calmodulin contrary to haemoglobin does not carry Ca2+ itself but the information encoded in the Ca2+ wave. Therefore, Calmodulin is not proteinophobiac but needs to interact with numerous partners. Others CaBPs are more rigorous in theirs behaviors. Maybe, from a sociological point of view, this fact may ex-plain why “who is working on what”.

Thanks to Ulrike Stein who saved the session and maybe the financial burden of the future ECS meetings, by showing that you can use small molecules interacting with S100A4 to tackle colorectal cancer metasta-sis. Now, the proteins of the Ca2+ toolkit are also therapeutic targets. Let come, pharma-ceutical companies, to support our ECS meeting.

Finally, our Japan colleague, Hideki

Shibata, makes a link between the CaBP alg2 and the regulation of exocytosis. This penta EFhand domains protein is astonishing and allows getting some insight on the trans-duction of Ca2+ signals, avoiding being always below the same lantern, the calmodulin one. This session was well balanced and it was a real pleasure for me to chair it, al-though I did not like the ghost LARSEN whis-pering around in this old building.

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Jacques Haiech

The Sunday afternoon was well filled as at 18h00 the second session started, com-pletely devoted to mitochondrial Ca2+ han-dling. Mitochondrial Ca2+ handling is an im-portant determinant of cell fate including apoptosis and autophagy and is therefore the subject of intense investigations. After a brief introduction recapitulating the first findings concerning mitochondrial Ca2+ uptake (dating back from the 50’s and the 60’s of last cen-

tury!), the importance of the seminal finding published in the early 90’s, of Rizzuto and

colleagues that the endoplasmic reticulum (ER) and mitochondria can associate and form microdomains was highlighted. A multi-tude of proteins play a role in the formation of those microdomains and in regulating the up-take and release of mitochondrial Ca2+. Sur-prisingly, the main Ca2+-transport proteins of the mitochondria were only very recently identified and molecularly characterized (the Na+/Ca2+ exchanger NCLX in 2010 by the group of I. Sekler; the mitochondrial Ca2+ uni-porter MCU by the groups of Rizzuto and Mootha). The characterization of these vari-ous proteins now opens new avenues for in-vestigation.

The keynote lecturer was Dr. Rosario Rizzuto (Univ. Padova, Italy) who first de-scribed in detail the strategy used to identify and characterize MCU, and subsequently dis-cussed his new finding of a MCU isoform dubbed MCUb who has no channel properties but instead inhibits Ca2+ influx. The second

lecturer was Dr. Gyorgi Szabadkai (Univ. College London, UK) who stressed the impor-tance of the ER-mitochondria relation during ER stress and in particular how ER stress regulates mitochondrial function and survival and how Ca2+, by acting on the ATP-ADP transporter SCaMC-1, modulates Ca2+ buffer-

ing into the mitochondria. The third speaker

was Dr. Varda Shoshan-Barmatz (Univ. Negev, Israel). She described the properties of the VDAC1 channel in the outer mitochon-drial membrane, its Ca2+-mediated oligomeri-zation and its role in cytochrome c release. From the many excellent posters sub-mitted to this session, two were chosen for oral presentation. A first was presented by Dr.

Geneviève Dupont (Université Libre de Bruxelles, Belgium) who presented collabora-tive work performed together with a group in Switzerland and a group in France. Together they demonstrated that Hint2 affects mito-chondrial Ca2+ dynamics and subsequent apoptosis by affecting the electron transport

chain. The final presentation was by Dr. Ma-risa Brini (Univ. Padova, Italy), who pre-sented new data on the role of Pink1 and Parkin on mitochondrial Ca2+ homeostasis. These proteins play a role in the mitophagy of defective mitochondria and can be mutated in Parkinson’s disease. Interestingly, these pro-

teins can also affect Ca2+ uptake in the mito-chondria at least in part by modulating ER-mitochondria tethering. Due to the many questions asked to the different speakers, the session closed with a slight delay but happily al participants could then directly enjoy drinks and snacks at the Welcome Party in the “Salle des Colonnes”.

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Mitochondrial Calcium homeostasis by Jan Parys

Jan Parys & colleagues during the open bar –

poster session

The aim of this session was to give an overview of the mechanisms involved in memory formation and how a dysfunction of these mechanisms can induce neurodegen-erative diseases.

The first talk gave by Graham Collin-gridge reminds us that the hippocampus is one of the most important region where the memory is formed and the informations are stored. The memory formation seems to re-quire long-term potentiation (LTP) and long-term depression (LTD). Glutamate receptors, called NMDA, triggers the LTP at hippocam-pal synapses via Ca2+ increase. However, Ca2+ is a transient signal so how can it main-tain the potentiation. The response to this question may be found in the fact that LTP involved Ca2+ release from intracellular stores and also the activation of different Ca2+-sensitive protein kinases. LTD process also involved Ca2+ release from stores but the sig-naling pathways are different.

Grace Stutzmann demonstrates that the disruption of neuronal Ca2+ signaling can induce neurodegenerative diseases such as Alzheimer’s disease (AD). An increase of

Ca2+ release mediated by ryanodine recep-tors (RyR) is observed in neurons from AD mice. This effect is due to an upregulation of type 2 RyR expression in presymptomatic AD mice. According to Cecilia Hidalgo talk, these RyR2 are also implicated in hippocampal-dependent memory processes such as spatial memory formation. So, a question still re-mains: have RyR2 got a good or a bad role? Thus, this confirms that the source of Ca2+ could be as important as the Ca2+ signal shape in this question. In Hilmar Bading’s talk, Ca2+ is presented as the “good guy” and the “bad guy”. Thus, Ca2+ can promote survival, generate memory but in

some case, Ca2+ can also kill the neurons. The magic role of NMDA receptors presented earlier is darkened by the fact that activation of NMDA receptors can kill neurons. The function of NMDA receptors depends on their location. The activation of extrasynaptic NMDA receptors induces cell death whereas activation of synaptic NMDA receptors keeps the neurons healthy. The major difference between these two processes is that synaptic NMDA receptors induce nuclear Ca2+ signal-ing. Nuclear Ca2+ activates expression of neu-ronal genes which are targets of the CREB/CBP transcription factor complex. Imaging of nuclear Ca2+ in the living fruit fly brain during olfactory learning demonstrates that the for-mation of long-term memory requires nuclear Ca2+ signaling. The balance between extra-synaptic and synaptic NMDA receptors could be a key point that needs to be explored in some neurodegenerative diseases. Finally, the last talk gave by Almudena Albillos shown that studies of other receptors such as nico-tinic receptors are important as they could also be involved in neuronal diseases.

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Session/

Memory & Neurodegenerative diseases by Valérie Raymond

Valérie Raymond at the registration desk at the conference venue

Your body defend against pathogens via two ways. 1) The innate system in which macrophages and neutrophils provide the first line of defense against microorganisms. The cytokines and chemokines released by macrophages in response to bacterial con-stituents initiate the process known as inflam-mation. Inflammation is one of the first re-sponses of the immune system to infection allowing eliminating pathogens. 2) The adap-tive immune system, which is activated by the innate response, is antigen-specific. During adaptive immunity, antigens are transported to lymphoid organs where they are recog-nized by naive B-lymphocytes and T-lymphocytes. These activated B- and T-lymphocytes subsequently proliferate and dif-ferentiate into effector cells. The adaptive im-mune response triggers immunological mem-ory after an initial response to a specific pathogen, leading to an enhanced response to subsequent encounters with that same pathogen.

The speakers approached several as-pects of calcium (Ca2+) signalling in immune

cells. Stefan Feske spoke about the couple STIM/ORAI in infection and autoimmunity. In T lymphocytes, the best described Ca2+ sig-nalling involves a depletion of ER Ca2+ stock that is sensed by STIM, which relocalize near the plasma membrane to activate the ORAI Ca2+ channels responsible for a sustained Ca2+ increase. T lymphocytes from patients with homozygous autosomal recessive muta-tions in STIM1 or ORAI1 genes have a strong reduction in the entry Ca2+ upon activation. S. Feske showed us data demonstrating the role of STIM and ORAi in infection and autoimmu-nity. Virus-specific CD8 T cells fail to persist in STIM deficient mice which are associated

with an absence of memory immune re-sponse against this virus. Mice with T-cell-specific deletion of STIM1 and STIM2 were protected from induction of experimental autoimmune encephalomyelitis (EAE), a murin model of multiple sceloris. This resis-tance is characterized by a failure of effector T cells to expand and accumulate in central nervous system and lymph node and in a de-

crease of IFNg and IL-17 productions. These

data demonstrate that both STIM and ORAI are critical for T-cell function and autoimmu-nity in vivo.

François Rassendren reported the role of purinergic receptor in inflammation and pain. P2X receptors (P2XR) are ATP-gated channels with high Ca2+ permeability. They have a widespread expression outside of the central nervous system and P2X4R and P2X7R have a prominent expression in innate immune cells. F. Rassendren studied the con-tribution of these receptors in inflamation us-ing P2X4R-deficient mice. These mice display reduced inflammation pain and an impaired production of prostaglandin (PG) E2, the main PG produced during inflammation. The macrophages are identified as the main cell-type responsible of PGE2 production induced by P2X4R. Then, P2X4R has key receptors mediating inflammatory PGE2 release in vivo supporting their specific involvement in in-flammation.

Lucette Pelletier focused on Ca2+-voltage dependent channel in effector T lym-phocytes and especially those responsible for asthma. In addition to the couple STIM/ORAI, several groups reported the presence of volt-age-dependent Ca2+ channels (Cav1) in T lymphocytes. L. Pelletier demonstrated the selective expression of Cav1.2 and Cav1.3 in

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Session/

Calcium, inflammation and stress by Magali Savignac

Th2 lymphocytes (and not in Th1 cells). Th2 cells are responsible of asthma. Then, using Cav1-specific oligonucleotides antisense she shows that the inhibition of Cav1 channels reduced the development of experimental asthma. From a therapeutic point of view, it is interesting to note that human Th2 cells ex-press Cav1 channels and their inhibition in-duces a decrease of the calcium signal and cytokine production induced by TCR engage-ment. The question that remains unresolved is how these channels activated by depolari-zation in excitable cells, are activated in non-excitable cells.

Heidi Wolfmeier shown how cells de-fend against pore-forming toxins produced by pneumococcus. The pathogens gain access to host cells by secreting pore-forming toxins, which lead to the formation of trans-membrane pores. Nucleated cells have devel-oped mechanisms to inhibit the disruption of their plasma membrane. H. Wolfmeier showed that pneumolysin (PLY), the pore-forming toxin produced by all Streptococcus pneumoniae, induces Ca2+ influx, which in-duces the translocation of the Ca2+-sensitive proteins of the annexin family to plasma membrane to neutralize theses pores. She demonstrated the dual role of Ca2+ in this phenomenon: localized increase in Ca2+ near of pores induces repair of these pores, a global Ca2+ increase switches off the repair.

Andreas Guse demonstrated the role of the second messenger NAADP during autoimmune encephalomyelitis. Nicotinic acid adenine dinucleotide phosphate (NAADP) is a Ca2+-mobilizing second messenger that binds to and opens Ca2+ channels on intracellular organelles, thereby increasing the intracellu-lar Ca2+ concentration. Using NAADP antago-nist, A. Guse showed that the incidence and severity of clinical EAE was reduced in treated-mice, diminishing the recruitment and the activation of auto-aggressive effector T cells.

Trevor Shuttleworth discussed about how STIM1 activates the ARC channel. The arachidonic acid (AA) regulated Ca2+ chan-nels (ARC) are formed by as a heteropen-tamer of three ORAI1 and two ORAI3 sub-units. At the difference of CRAC channels, ARC channels are activated by the pool of STIM1 constitutively resident in the plasma membrane and independently of intracellular Ca2+ stock release. The expression of STIM1 mutant constitutively localized to plasma membrane by Lck-domain is sufficient for the AA-induced activation of ARC channels with-out the activation of CRAC channels.

This session deals with the great di-versity of Ca2+ responses and Ca2+ actors that control a large panel of functions in diverse immune cells. Beyond STIM/ORAI that plays an unquestionable role in the Ca2+ response of T-lymphocytes, other Ca2+ channels or regulators of the Ca2+ responses contribute to the singularities of the immune responses. A better understanding of how these compo-nents act to generate a given Ca2+ signature and how this signature is translated in terms of function would be of considerable thera-peutic interest. Indeed, this could lead to the design of more specific targets in the treat-ment of immune disorders while avoiding global immunosuppression.

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Magali Savignac chairperson of session on Ca2+ inflammation & stress

The session was devoted to the role of Ca2+ in development, which is a complex sequence of events that begins with fertiliza-tion and is followed by repeated rounds of cell proliferation to build up all the cells necessary to create a new organism. As the cell mass increases, cell specification mechanisms be-gin to allocate cells to form different functions and these begin to appear through a proc-esses of differentiation, which includes the creation of stem cells used for tissue repair and renewal in the adult. Many of these as-pects were described during the course of

this session. Khaled Machaca described the nature of the Ca2+ transients that initiate fertili-zation in many species. The Ca2+ oscillations that occur for 2 hours following fertilisation of mammalian oocytes are maintained by the Orai1 and STIM1 Ca2+ entry system and this observation may play an essential role in the oscillatory mechanism. The proliferation proc-esses that occur during subsequent develop-ment are also regulated by Ca2+ as was de-

scribed by Sarah Brennan in the case of vas-culogenesis in the developing foetal lung. She showed that the lung epithelium express volt-age-sensitive Ca2+ channels (L- and R-type) that may provide the Ca2+ signal necessary for proliferation. Such a role for voltage sensi-tive channels in a non-excitable cell resem-

bled that described by Lucette Pelletier for Th2 cells that use CaV1 channels to regulate airway inflammation. These two observations raise an interesting question concerning the nature of the voltage-independent mechanism responsible for activating these channels.

During development, Ca2+ described how Ca2+ plays a critical role in large scale morphogenetic movements that are driven by

activation of the cytoskeleton. Benjamin Bonneau described how Nrz, which belongs

to the Bcl-2 family, regulates this processes by controlling Ca2+ release from the IP3Rs. This inhibitory action depended on both the BH4 and BH1 domains of Nrz and highlighted the importance of the Bcl-2 family in regulat-ing Ca2+ signalling in processes other than apoptosis. Perhaps one of the most complex final events of differentiation is the wiring up

of the neural circuits in the brain. Christian Lohmann described how spontaneous flashes of Ca2+ localized to small regions of the dendrites drive connectivity. Such con-nections between pre-and postsynaptic sites tended to cluster to certain regions suggest-ing that each neuron makes multiple connec-tions to localized dendritic regions of each target neuron. A major unsolved problem con-cerns the nature of the spontaneous bursting activity responsible for the periodic release of neurotransmitters that is driving this connec-tivity.

Stem cells that are set aside during development are used in adult life for various repair processes as occurs in skeletal muscle where satellite stem cells are induced to pro-liferate during muscle damage to form pro-genitor cells that then fuse to form new mus-cle fibres. The mechanism responsible for this fusion process is still somewhat mysterious.

Fabrice Antigny provided evidence that the Ca2+ signal for fusion depends on TRPC1 and TRPC4 through a mechanism that may also require interleukin-13.

A significant feature of development concerns the stability of the differentiated cell phenotype. There are increasing numbers of examples of de-differentiation where cells lose their differentiated state and this can have both beneficial and pathological conse-

quences. In his keynote lecture, David Barker described how the root hairs in plants

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Session/

Calcium, Development and Stem cell by Michael Berridge

can alter their function to form nodules, which are nitrogen-fixing organs. This transforma-tion depends on a fascinating interplay be-tween the bacterium and the cells of the root- a dialogue that is orchestrated by a panoply of Ca2+ oscillations. A fascinating aspect of these oscillations is that they are located in the nucleus and there also are dramatic changes in frequency during various stages of the plant-microbe interaction. An example where de-differentiation has pathological con-

sequences is in malignancy. Bela Papp de-scribed how the expression of the Ca2+ pump SERCA3 may be a marker of cell differentia-tion and its progressive loss is correlated with the severity of breast and colon malignancies as the cells de-differentiate. There was no compensatory increase in the expression of SERCA2 and this raises the interesting possi-bility that there may be a parallel elevation in intracellular Ca2+ that could contribute to ma-lignancy.

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Michael Berridge

Join the ECS!

The aim of the ECS was and is to develop and sustain relationships between the scientists working in the field of calcium binding, calcium signalling and the study of the various proteins thereby involved (the "calcium toolkit").

If you are already member of the ECS don’t forget to renew your registration. Try to recruit new members Register your post docs. It is the best Christmas gift!

Junior researchers are especially supported by highly discounted rates at all ECS activities and the attribution to them of travel grants and poster prizes.

You have the possibility to make free donations that even can be tax-deductible.

For more details contact Jan Parys:

jan.parys@med.kuleuven.be

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For this 12th Meeting of the ECS in Toulouse, 12 fellowships sponsored by ECS were

awarded to young students from all over the world; Abhishek Aggarwal (Austria), Sumita Chakraborty (India), Marijke De Bock (Belgium), Uliana Levin Gromiko (Israel), Fernanda Magalhaes Ferrao (Brasil), Milena Milosevic (Serbia), Kanae Osugi (Japan), Elena Pera (Australia), Alexey Shalygin (Russia), Carlos Alejandro Toro (Chile), José Miguel Vicencio (UK), Hellen Jannisy Vieira Beiral (Brasil). The Best Poster Awards sponsored by ECS was to Elke Decrock from Belgium: for the poster entitled: Apoptosis converts IP3 into a pathological messenger that propa-gates intercellular apoptosis spread and to Cecilia Cheval from France for the poster enti-tled: Functional analysis of PRR2, a nuclear target of a calcium sensor (CML9) involved in plant defence against Pseudomonas syringae in Arabidopsis. The Best Poster Award in the session Calcium imaging (sponsored by the GDRE and Nikon) was to Takeharu Nagai from Japan for the poster entitled: Revolutionary bioimaging with super-duper lumines-cent proteins. The Drabikowski Award for the best short presentation selected from submitted ab-

stracts was obtained by Benjamin Bonneau from Dr Germain Gillet Lab (Lyon, France) for the oral presentation entitled: Regulation of Ca2+ fluxes by the anti-apoptotic protein NRZ dur-ing zebrafish development.

The 12th Meeting Awards

All the ECS fellows and Awards with Roland Pochet, Jacek Kuznicki

and Stephen Moss

Some ECS fellows with Roland Pochet

It was a great pleasure for me to at-tend the 12th symposium of the European Calcium Society in Toulouse, facilitated by the travel fellowship I received from the or-

ganizers. Since I had never attended a Ca2+ specific meeting before this conference prom-ised to be a valuable experience for my ca-reer and a perfect venue to present my work.

Thanks to this meeting I had the op-portunity to meet distinguished scientists and discuss with them, my work on “The role of

the Calcium Sensing Receptor in colorectal cancer proliferation”. The programme of the

ECS 2012 was impressive, covering a wide range of topics. During the conference I have gained a wide insight into the different as-pects of intracellular Ca2+ signalling. I really appreciated Prof. Daniela Riccardi’s invited

lecture during the opening day, which was a brilliant start for the amazing talks presented during the meeting and Prof. Anjana Rao’s

closing talk, which beautifully concluded the 3 day event.

The international mix of high profile scientists offered interesting sessions with fruitful discussions. I particularly enjoyed talk-ing to other attendees at the poster sessions in a lively and interactive environment. This event was a fantastic opportunity for meeting

other researchers and making new contacts or just for social interaction – the organizers took the extra effort to ensure that the social evenings were enjoyed by all, right from a very enjoyable evening at the Mayor Hall Re-ception, to the brilliant wine and dine ‘Gala

Dinner’. For students like me, who are in their

early stages of their scientific career, the ECS meetings are very appropriate not only to es-tablish relationships with the scientific com-munity who work closely with the science of Ca2+ signalling but the small size of these meetings makes it very comfortable and ac-cessible to discuss one’s science.

I would like to thank the ECS organiz-ers for giving us, the ‘calcium enthusiasts’

such an opportunity to open myself to novel working perspectives and identifying new col-laborations.

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General impressions on the 12th ECS Meeting

by Abhishek Agggarwal (one laureate of the travel fellowship)

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12 September 2012, the meeting is over

See you in 2014

Highlights of the meeting

EC

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Wor

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ECS workshops

More details very soon!

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Post-doc position available

In a pioneering international initiative, Cornell University and Weill Cornell Medical College es-tablished the Weill Cornell Medical College in Qatar (WCMC-Q) through a unique partnership with the Qatar Foundation for Education, Science and Community Development. Located in Doha, Qatar, and entering its eleventh year of operation.

The Machaca laboratory at WCMC-Q seeks candidates for two postdoctoral associate positions

1- SOCE During Cell Division to study the regulation of store-operated Ca2+ channels during cell division

2- Trafficking in Xenopus Oocytes to study the trafficking of membrane proteins during Xenopus oocyte maturation.

The successful candidates should hold a Ph.D. and have broad expertise in molecular, bio-chemical and/or cellular imaging approaches. The Lab is interested in mechanisms mediating meiotic arrest and the resumption of the mei-otic cell cycle in Xenopus. In addition we are interested in the regulation of ion channels and transport pathways during cellular development, with a primary focus on the regulation of Ca2+ signalling during oocyte maturation and during mitosis. More details about the Lab are available at: http://qatarweill.cornell.edu/research/faculty/machacalab.html WCMC-Q is located in Education City among other American universities in Doha, which is a rapidly growing research hub. The WCMC-Q research program offers a collaborative, multidis-ciplinary team environment, endowed with a comprehensive support infrastructure. Details re-garding the WCMC-Q research program and facilities can be accessed at http://qatarweill.cornell.edu/research/index.html. WCMC-Q postdoctoral associates are appointed by the academic departments at Weill Cornell Medical College. Salary is commensurate with experience and is accompanied by an attractive foreign-service benefits package, including paid housing and a car allowance. Qualified applicants are invited to submit a letter of application, which should outline their inter-est in the position, along with their curriculum vitae including the names and contact details of

three referees, to http://job.qatar-med.cornell.edu Positions are open until filled. Please note that, due to the high volume of applications, only short-listed candidates will be contacted. Cornell University is an equal opportunity, affirmative action educator and employer.

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Post-doc position available

PhD position available in the laboratory of Nicolas Demaurex, University of Geneva, Department of Cellular Physiology and Metabolism.

We are looking for motivated PhD candidates with a keen interest in cell biology or biomedical sciences. The program provides in-depth, multidisciplinary training in biomedical research in a stimulating international environment. Ca2+ is a ubiquitous second messenger that plays numerous roles in many aspects of physiol-ogy. The immune system is particularly sensitive to mutations in molecules involving store-operated Ca2+ entry pathways, and understanding the role of these molecules is paramount to the development of novel therapies for immunodefiencies and autoimmune diseases. The the-sis project will focus on dissecting the mechanisms of store-operated Ca2+ entry regulator STIM1 in various cellular models including phagocytic immune cells such as neutrophils. Can-didates will gain expertise in various aspects of cell biology and biomedical sciences using a wide spectrum of cellular and biochemical techniques with heavy emphasis on live-cell imag-ing.

Qualifications: Applicants must hold an undergraduate degree equivalent to a master of sci-ence in any discipline of natural or life sciences or medicine. Experience with common tech-niques in biochemical, molecular and cellular biology, and particularly with imaging techniques are appreciated. Proficiency in French is not necessary. Terms: PhD student position is for 3-4 years starting Fall 2012 (approximate salary: 45’000 CHF/ year)

Applications: The deadline to submit applications is the 15th Oct 2012. Please send your ap-plication including CV, postgraduate transcripts, a brief statement of research experiences and interests, and the names and contact information of 2 references. Selected candidates will be invited for a short presentation (in english) and an interview.

References: Nunes P, Cornut C, Bochet V, Hasler U, Oh-Hora M, Waldburger JM, & Demaurex N. STIM1 juxtaposes ER to phagosomes, generating Ca2+ hotspots that boost phagocytosis. Current Biology (in press). Shen WW, Frieden M, Demaurex N. Local cytosolic Ca2+ elevations are required for stromal interaction molecule 1 (STIM1) de-oligomerization and termination of store-operated Ca2+ en-

Adresse

Nicolas.Demaurex@unige.ch

Nicolas Demaurex Dept. of Cellular Physiology & Metabolism Faculty of Medicine, University of Geneva Centre Médical Universitaire, 1 rue Michel-Servet CH-1211 Geneva 4, Switzerland Tel.: +41 (22) 379 53 99 Fax: +41 (22) 379 52 60

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We are organizing the 10th International Calreticulin Workshop in Banff, Alberta,

Canada in April 10-13, 2013, (www.crt2013.com). The workshop will take place in a spectacular location at the historic Banff Springs Hotel, close to an outstanding skiing area and other local attractions. The cost for the whole conference, all inclusive, will be approximately $950 per person based on double occupancy. The 2013 Workshop en-compasses broad areas of biology including protein folding and quality control in the ER, calcium homeostasis, cell adhesion, wound healing, heart disease, cancer and autoimmunity, and the pathology of protein folding diseases.

For additional information please contact:

marek.michalak@ualberta.ca.

We look forward to seeing you in Banff next year.

10-13 April , 2013, Banff,

Canada

11-13 September , 2013, Leuven, Belgium

contact: jan.parys@med.kuleuven.be

And do not Forget the ECS Workshops

20-22 October , 2013, Logonna-Daoulas, France

contact: olivier.mignen@univ-brest.fr

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New Board

Composition of the Board, since the General Assembly of September 11th, 2012

(Toulouse meeting)

President Dr. Marc MOREAU

Vice-President

Dr. Catherine LECLERC

Secretary Prof. Jan B. Parys

Treasurer

Prof. Roland POCHET

Board members Prof. Volker GERKE

Prof. Claus HEIZMANN Dr. Jacek KUZNICKI Prof. Steven MOSS

Prof. James W. PUTNEY Jr

Claude B. Klee Michael Berridge Claus Heizmann

Katsuhiko Mikoshiba R.J.P. Williams

At the last General assembly it has been proposed as new honorary members

Erwin Neher Rosario Donato Jacques Haiech

For these new members a CV will be available

in the next issue (May) of the newsletter

New

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TheThe President writesPresident writes

I would like to thank Steve Moss for the job accom-plished as President during these last years. I’ll try to

do the best to pursue this work to increase the devel-opment of the ECS. The board has been modified dur-ing the last general assembly in Toulouse. Three hon-orary members have been proposed Rosario Donato, Jacques Haiech who belong to the founder team of the ECS and Erwin Neher. I am very happy of this deci-sion.

The visibility of ECS is growing up and we begin to attain a critical mass. In 2010 we were 171 members and at the end of 2012 we are 256. It is only the begin-ning we hope to recruit outside of the Europe. I hope that Jim Putney our new board member will be able to bring the colours of the ECS in US.

The scientific activity of the ECS is increasing, in 2013 two workshops are planned in the next autumn, one in Leuven (Belgium) Ca2+ and cell death and the one other in a small village close to Brest (Brittany,France) on the following topic Ca2+ signalling as a hub for translational medicine and a starting point to model life (see the announcements in this letter). Don’t be afraid

autumns are fine In Leuven and in Brittany too.

This letter is yours; don’t forget to send to Catherine

Leclerc (catherine.leclerc@univ-tlse3.fr) informations, scientific debates, new findings, comments of articles etc…

Wishing you all, a nice end of 2012 and a happy new year, I hope you will enjoy with this new issue.

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The previous and new president of the ECS, Stephen Moss and Marc Moreau, discussing with Claus Heizmann during

the gala diner in Toulouse

A peaceful moment for Stephen Moss during

the ECS meeting 2012