Seminars at the CABD

Unless specified, all seminars are held at noon in the seminars room. You can find information regarding our upcoming seminars in the following calendar:

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Previous seminars: 

CABD Seminar December 11 @ 11:00 am
Primate and human evolution
Dr. Tomas Marqués-Bonet
ERC, Barcelona

CABD Seminar December 4 @ noon
Contracting, Spreading, folding: How cellular forces can shape biological tissues during development
Dr. Jerome Solon
CRG, Barcelona

Summary: During embryogenesis, dramatic tissue reorganization occurs under the control of specific signaling pathways. Mechanical forces are coordinated in order to rearrange biological tissues and shape organs. The mechanisms at the origin of the generation and regulation of these forces during development remain elusive. My group is interested in understanding how fundamental modes of tissue remodeling such as epithelial contraction, tissue spreading or folding are regulated during development. Here, I will present recent works on the generation and regulation of forces during tissue contraction and show an unusual contractile mechanism involving apoptosis in Drosophila dorsal closure. I will also discuss new results on the mechanisms promoting spreading of epidermal tissues and ensuring positional control in the process of Drosophila head involution.
CABD Seminar November 13 @ noon
Evolution of gene regulation in 20 mammals
Dr. Diego Villar
University of Cambridge & CRUK - Cambridge Institute, UK

Summary: The mammalian radiation has corresponded with rapid changes in the noncoding genome, but we lack a comprehensive understanding of regulatory evolution in mammals. While comparison of whole-genome sequences across many mammalian species has revealed evolutionarily constrained non-coding elements (many of which are likely regulatory elements), experimental binding locations of transcription factors and histone marks have been shown to evolve rapidly, suggesting that there is limited correspondence between non-coding sequence conservation and regulatory function. To experimentally dissect the evolution of mammalian regulatory regions, we tracked promoters and enhancers active in liver tissue across twenty species of mammals by profiling genomic enrichment of H3K27 acetylation and H3K4 trimethylation. We report rapid evolution of enhancers as a universal feature of mammalian genomes: across all study species half of all liver enhancers are unique to a single species. Most of these recently-evolved enhancers arise from exaptation of ancestral DNA, and not from lineage-specific expansions of repeat elements. In contrast, almost all liver promoters are partially or fully conserved across our study species. Recently-evolved enhancers can be associated with genes under positive selection, demonstrating a powerful approach to annotating potential regulatory adaptations in newly sequenced genomes. These results provide unprecedented insight into the functional genetics underpinning mammalian regulatory evolution.
CABD Seminar November 12 @ 11:30am
MicroRNA in cancer
Prof. Gerolama Condorelli
Department of Molecular Medicine and Medical Biotechnology , Federico II University of Naples, Italy

Summary: Despite many novel therapeutic approaches, breast cancer remains one of the leading causes of cancer mortality among women. Recent findings indicate that cancer-associated fibroblasts (CAFs), the major components of the tumor microenvironment, play a crucial role in breast cancer progression, but how they promote tumorigenesis is poorly understood. Increasing evidence indicates that exosomes, membrane vesicles sized 30-100 nm in diameter, may vehicolate their cargo, including microRNAs (miRs), thus affecting the biological behaviour of recipient cells. Therefore, one alternative mechanism of the promotion of breast cancer progression by CAFs may be through cancer-associated fibroblast-secreted exosomes, which would deliver oncogenic miRs to breast cancer cells. In order to investigate the potential role of miRs in stroma-tumor communication, we profiled miR expression in exosomes from cancer-associated fibroblasts compared to normal fibroblasts. We found that in CAF exosomes the levels of miR-21, miR-378e, and miR-143 were increased as compared to normal fibroblast exosomes. By immunofluorescence experiments, we demonstrated that PKH26-labeled-exosomes could be transferred from fibroblasts to T47D breast cancer cells. Furthermore, we elucidated that cy3-labeled-miRs (cy3-miR-21, cy3-miR-143, cy3-miR-378e) were shuttled into T47D cells via CAF exosomes. Moreover, for the first time, we provided evidence of the role of CAF exosomes and their miR contents in the induction of the stemness phenotype in different breast cancer cells, BT549, MDA-MB-231 and T47D. We also studied miRs effects on tamoxifen resistance. We conclude that CAFs strongly promote the development of an aggressive phenotype of breast cancer cells through exosome-mediated delivery of these oncogenic miRs.
CABD Seminar November 6 @ noon
Control of intercellular forces and epithelial dynamics by the adhesome
Dr. Xavier Trepat
IBEC, Barcelona

Summary: A broad range of biological processes such as morphogenesis, tissue regeneration, and cancer invasion depend on the collective dynamics of epithelial cells. Such dynamics are determined by an exquisite balance between intercellular adhesion, cytoskeletal tension, and intracellular pressure. To study this balance in a fully quantitative manner I will present new techniques to map physical forces between and within cells. Using these techniques we studied how cellular forces are regulated and transmitted by the proteins that comprise intercellular adhesion complexes. To do so, we perturbed the main molecular players of the intercellular adhesome using RNAi and studied how these perturbations impact physical forces and cellular velocities in epithelial cell collectives. We found that perturbations targeting adherens junctions, but also tight junctions, gap junctions, and desmosomes have a significant impact on cell velocities, cell deformations, cell-matrix traction forces, and cell-cell forces. We developed a cross-validation analysis to show that concentrations of cell-cell adhesion proteins are significant predictors of cell-cell forces. Finally, I will discuss how cell-cell forces mediate cancer cell invasion led by cancer associated fibroblasts.
CABD Seminar Oct 23 at 11am
Muscle stem cell regenerative decline in aging
Dra. Pura Muñoz
ICREA, Universitat Pompeu Fabra, Ciberned, Barcelona

Summary: Our group aims to understand the mechanisms regulating stem cell homeostasis and regenerative functions: how stem cells maintain quiescence, are activated, transit to proliferative expansion and differentiation, and finally self-renew, and how they interact with the external inflammatory environment. Research is specially focused on stem cells of skeletal muscle. Recent studies from the laboratory have shed light on 1) age-associated muscle decline and wasting (sarcopenia) and loss of stem-cell regenerative functions with aging; and 2) the physiopathology of muscular dystrophies, with a specific interest in the contribution of inflammation and fibrosis to dystrophy progression. These findings are relevant for regenerative medicine.
CABD Seminar September 25@ noon
Building Muscle Tissue from Two Hundred Cells
Dr. Simon Hughes
King's College, London

Summary: The zebrafish somite forms a diverse set of muscle fibres and stem cells for later muscle growth. Work from a small group of labs worldwide has elucidated mechanisms controlling these events.  We are now interested in how later muscle growth is regulated.  Our current studies on the molecular and cellular basis of growth control, homeostasis and wound repair will be described. 
CABD Seminar September 18 @ noon

Dr. Laura van Niftrik
Department of Microbiology Institute for Water & Wetland Research Radboud University, Nijmegen
CABD Seminar September 11@ noon
C. elegans towards the genetic dissection of biological timing.
Dr. María Olmedo
CABD Seminar July 3 @ noon
Mitotic control of the nuclear membrane
Dr. Snezhana Oliferenko
King's College London, UK

Summary: Mitotic control of the nuclear membrane" The nuclear membrane must remodel during mitosis to accommodate mitotic spindle assembly, chromosome partitioning and formation of the daughter nuclei. This can be accomplished through a variety of strategies, ranging from “open” to fully “closed” mitotic division. During open mitosis, the envelope of the original nucleus breaks down in prophase and reassembles around the segregated daughter genomes. In closed mitosis, the nuclear envelope remains intact throughout chromosome segregation. We have shown that within the fission yeast clade, the mitotic control of the nuclear surface area may determine the choice between the nuclear envelope breakdown and a fully closed division. I will present our recent work on the mechanistic basis of this divergence and argue that comparative and synthetic cell biology studies using two fission yeast species could provide unique insights into physiology and evolution of mitosis.
CABD Seminar June 19 @ noon
Theoretical approaches to stem cell differentiation
Dr. David Míguez
Facultad de Ciencias, UAM, Madrid

Summary: The understanding of the regulatory processes that orchestrate stem cell maintenance is a cornerstone in devel- opmental biology. We present a mathematical model based on a branching process formalism that predicts average rates of proliferative and differentiative divisions in a given stem cell population. In the context of vertebrate spinal neurogenesis, the model predicts complex non-monotonic variations in the rates of pp, pd and dd modes of division as well as in cell cycle length, in agreement with experimental results. Moreover, the model shows that the differentiation probability follows a binomial distribution, allowing us to develop equations to predict the rates of each mode of division. A phenomenological simulation of the developing spinal cord informed with the average cell cycle length and division rates predicted by the mathematical model reproduces the correct dynamics of proliferation and differentiation in terms of average numbers of progenitors and differentiated cells. Overall, the present mathematical framework represents a powerful tool to unveil the changes in the rate and mode of division of a given stem cell pool by simply quantifying numbers of cells at different times.
CABD Seminar June 12 @ noon
Tumorigenesis in Drosophila, “Tumor Hotspot” hypothesis
Dr. Wu-Min Deng
Biological Sciences, Florida State University, USA

Summary: Malignant tumors are caused by uncontrolled proliferation of transformed mutant cells that have lost the ability to maintain tissue integrity. Although a number of causative mutations for oncogenes or tumor-suppressor genes have been discovered, the initial steps mutant cells take to escape cellular defense mechanisms and trigger tumorigenesis remain unclear. In our analysis of conserved neoplastic tumor-suppressor genes (nTSGs) in Drosophila imaginal epithelia, we identified a specific region in which tumorigenesis always originates. In this “tumor hotspot,” nTSG mutant cells delaminate from the apical side of the epithelia and undergo tumorigenic overgrowth. Conversely, in other regions dubbed “tumor coldspots,” nTSG mutant cells are outcompeted by their wild-type neighbors, causing them to be basally extruded and undergo apoptosis. Further analysis of cytoarchitectural differences between the coldspots and hotspots revealed intrinsic cellular structures observed specifically in the tumor hotspots. The hotspot-specific cytoarchitecture prevents the nTSG mutant cells from being extruded from the basal side and promotes their apical delamination. We show that the apically delaminating nTSG mutant cells exploit the endogenous growth promoting signaling activity for their survival and growth in the luminal region. Given the conservation of the epithelial cytoarchitecture, tumorigenesis could be generally initiated from tumor hotspots in a similar mechanism.
CABD Seminar June 5 @ noon
Identification of Internal ribosome entry site (IRES) by a new comparative genomic approach.
Dr Enrique Merino
UNAM, Cuernavaca, México

Summary: A common strategy of some viruses to ensure the selectively synthesis of their proteins whereas inhibit host proteins translation is the inactivation of eukaryotic initiation factors (eIFs). For example, in most picornaviruses infections, this inactivation is achieved by cleaving the eIF-4G by a specific viral protease, and therefore a cap-independent process achieves the translation of these viral mRNAs. Analysis of the 5´ UTRs of these mRNAs revealed that a common feature among them was the presence of highly structured RNA secondary structures, which became known as Internal Ribosome Entry Sites or IRES. It was then hypothesized that similar elements might be presences in cellular mRNAs which translation is required for stress survival and other physiological or development processes. At present, only a limited number of cellular IRES have been experimentally identified and the lack of primary sequence and mRNA secondary structure conservation has made their identification a difficult task. I will present a new comparative genomic method for the prediction of IRES in mammalian and fungal organisms and discuss a statistical analysis of their enrichment in stress-related orthologous groups.
CABD Seminar May 22 @ 11:45
Aplicaciones de la técnica de Resonancia de Plasmón de Superficie
Dr. Marta Taulés
Parque Científico de Barcelona
CABD Seminar May 15 @ noon
Deciding between making trunk or tail structures during vertebrate development
Dr. Moisés Mallo
Instituto Gulbenkian de Ciencia (IGC), Oeiras, Portugal

Summary: During development, the vertebrate body is made from head to tail by progressive addition of new tissue at its caudal end. Although this process is continuous, it can be divided in three distinct phases associated with the production of head, trunk and tail structures. All vertebrates go through these stages but their relative weight in the formation of the final body varies widely among species. Here, I will discuss the mechanisms controlling growth through the trunk region and the regulation of the transition from making trunk to producing tail structures. I will illustrate these mechanisms using genetic approaches to manipulate gene expression in mouse embryos.
CABD Seminar May 7 @ noon
Applying an optimized CRISPR/Cas9 system to uncover genes involved in human diseases
Dr. Miguel A. Moreno-Mateos
Department of Genetics Yale University School of Medicine

Summary: The human genome sequence was the entry point to understand the genetic bases of human diseases. Large-scale genome-association studies have further identified candidate genes associated with human diseases. Sharing high genetic similarity to humans, zebrafish is an excellent model organism to study the function of these genes and more generally vertebrate development. To this aim, genome editing systems to generate genetic models are essential. Recently, the CRISPR/Cas9 has recently emerged as a genome editing system. This targeting system is based on two components: a single guide RNA (sgRNA) that directs the Cas9 endonuclease to the target site to be mutated. However, the rules determining CRISPR/Cas9 targeting efficiency in vivo remain largely unknown. Here, we have carried out a large-scale analysis of the CRISPR/Cas9 activity in vivo using zebrafish embryos. This analysis revealed underlying sgRNA nucleotide preferences affecting CRISPR/Cas9 activity specifically in vivo. These novel findings have been integrated into a predictive model (CRISPRscan http://www.yale.edu/giraldezlab/Crisprscan.html). In addition, we have optimized a novel version of the CRISPR/Cas9 system that concentrates the mutations in the germ cells avoiding possible toxicity or lethality coming from mutations in the soma. This novel system allows for carrying out functional genetic screens in vertebrates in a rapid and efficient manner. Indeed, using our optimized CRISPR/Cas9 system in zebrafish, we identified a novel gene involved in vertebrate brain development that is mutated in a consanguineous family with primary autosomal recessive microcephaly (MCPH). MCPH is a rare neurodevelopmental disorder in children that results in decreases in cognitive abilities and a significant reduction in brain size. The uncovered gene has been involved in splicing in yeast and human cell lines but not well characterized in any in vivo vertebrate system. Currently, we are studying the molecular role of this gene and its relationship with brain development. In summary, our data provide novel insights into the determinants that mediate CRISPR/Cas9 efficiency and its application to uncover genes involved in human development.
CABD Seminar April 28 @ noon
Transcriptomics and epigenomics analyses of the development of the turtle shell
Dr Juan Pascual-Anaya
Evolutionary Morphology Laboratory, RIKEN, Japan

Summary: The turtle shell is a genuine morphological innovation within tetrapods. Its formation requires a complete anatomical distortion of the tetrapod body plan, resulting in an open, fan-like ribcage formed by plate-like ribs that eventually enclose the shoulder girdle (otherwise, remaining outside in the rest of amniotes). During development, the turtle shell is preceded by the formation of an ectodermal ridge, underlain by a condensed mesenchyme, running anterior-posteriorly through the dorsal flank of the body in the inter-limb region, the so-called carapacial ridge (CR). The CR is thought to control the development of the shell. In recent studies, we have shown the specific expression of key developmental genes in the CR, not expressed in the dorsal flank of chicken and mouse neither in the body wall of the turtle. These genes have probably been co-opted from other developmental modules (such as the limbs) and could have important functions in the shell development, at least regarding the correct fan-like disposition of the ribs. However, the whole gene regulatory network(s) controlling the formation of the CR remains a mystery. Here, I will present a comparative analysis of the CR and other structures (limbs and body walls) from the Chinese soft-shell turtle, Pelodiscus sinensis, and of homologous or equivalent embryonic regions of the chicken (dorsal flank, limbs and body walls), from RNA-seq and ChIPseq for 3 histone marks datasets. Our (inter and intra-species) comparative analyses allowed us to identify those genes that are expressed in the CR of P. sinensis, and that might be involved in the turtle shell development.
CABD Seminar April 10 @ noon
Transcription and nuclear organisation: cause and consequence
Wendy Bickmore
MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK

Summary: There are some well-established relationships between aspects of the spatial organisation of the nucleus and gene expression. Sequences at the nuclear periphery are often associated with the repression of transcription, the most active regions of genomes are often found in the centre of the nucleus, loci repressed by certain epigenetic pathways are found in a compact chromatin state. But who comes first: does structure direct function (transcription) or vice versa? I will describe experiments that try to break the links between chromatin/nuclear organisation - especially at the nuclear periphery - and the act of transcription. By regulating transcription using synthetic transcription factors, I will discuss the extent to which we can begin to understand the relationships between structure and function in the nucleus. In addition, I will use similar approaches to investigate how chromatin folding contributes to the activation of transcription from enhancers located distant from their target genes.
CABD Seminar March 27 @ noon
Genomic and proteomic analysis of MEF2 dependent transcriptional programs in cardiac and skeletal muscle
Dr. John McDermott
York University, Toronto, Canada

Summary: MEF2 plays a profound role in the regulation of transcription in cardiac and skeletal muscle cell lineages. To begin to fully define the overlapping and unique MEF2A targets in cardiac and skeletal myocyte lineages, we utilized high throughput ChIP-exo analysis of cultured cardiomyocytes and skeletal myoblasts. Of the 2783 and 1648 MEF2 binding peaks found in skeletal myoblasts and cardiomyocytes respectively, 294 common binding sites were identified. Genomic targets discovered by ChIP-exo were then compared to genes that were differentially expressed in RNA-seq analysis of MEF2A depleted myogenic cells. Differential analysis of genes up or downregulated in response to siRNA mediated MEF2A gene silencing in myoblasts revealed two prominent genetic networks. In addition to identifying the genomic landscape for MEF2 DNA binding, we also sought to identify the MEF2 interactome by Mass spectrometry based affinity purification methods (AP- LC-MS/MS) and this approach will be discussed. These data illustrate firstly that MEF2 orchestrates both common and non-overlapping programs of gene expression in skeletal and cardiac muscle lineages that are associated with several gene ontology processes, and secondly, that MEF2 fulfills an important regulatory function at a number of genomic targets as a suppressor of gene expression. These data imply that MEF2 dependent gene repression may be an important function of MEF2 in striated muscle lineage induction in addition to its role as a positive transcriptional activator of muscle structural genes.
CABD Seminar March 13 @ noon
Building the inner ear: cellular dynamics of neurosensory progenitors during embryonic development
Dr. Cristina Pujades
Department of Experimental and Health Sciences, Universitat Pompeu Fabra, Barcelona

Summary: All the cellular components of the inner ear, afferent neurons and both sensory and non-sensory epithelia, arise from the otic placode. This requires a tight coordination between morphogenesis and cell fate specification. We have recently shown that the otic neurosensory precursors may be composed of three populations: i) unipotent neuronal precursors that form only neurons, ii) sensory precursors that form only hair cells, and iii) bipotent precursors that give rise to both cell types. Now, we want to reconstruct the cell lineage of the otic progenitor cells and characterize their dynamics, including cell division, position, displacement, shape changes, identity and fate. To reach this objective, we performed SPIM live imaging of fluorescently labelled zebrafish embryos, and processed the 3D+time data. We show how first sensory hair cells develop and acquire their final position within the maculae sensory patches, and how they behave upon expansion of the bipotent progenitor pool. In addition we followed the dynamics of otic neurogenesis and delamination of neuroblasts, and analysed how time and place of birth affect neuroblast behaviour within the nascent statoacoustic ganglion (SAG). With this approach, we are able to build up the map of neurosensory progenitors within the otic primordium and follow their lineage.
CABD Seminar March 6 @ noon
Cis-regulatory mechanisms of HoxD gene expression and the origin of digits
Dr. Igor Schneider
Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, Brasil

Summary: The skeleton of tetrapod limbs is composed of three segments, stylopod, zeugopod, and autopod. This pattern has served as the basis for a remarkably broad adaptive radiation from wings and flippers to hands and digging organs. A central area of inquiry has been tracing the origins of the elements of this bauplan in the fins of diverse fish. Can equivalents of the three segments, and the developmental processes that pattern them, be seen in fish fins? To address this, we have focused on the comparative analysis of cis-regulation of Hoxd genes in fins and limbs. We find conserved regulatory mechanisms associated with the expression of Hoxd genes in limbs and fins that point to an ancient origin of a distal compartment in vertebrate appendages. The study of regulatory biology of developmental genes of diverse species offers novel data to investigate these classical questions.
CABD Seminar February 20 @ noon
The LINC complex: a nuclear-cytoskeletal connector and contributor to inherited muscular dystrophies
Dr. Sue Shackleton
Department of Biochemistry University of Leicester

Summary: The LINC (linker of nucleoskeleton and cytoskeleton) complex is located in the nuclear envelope and is comprised of 2 families: SUN and nesprin proteins. Together the proteins span the double membrane of the nuclear envelope and connect the nucleus to the cytoskeleton. This connection is vital for cellular resistance to mechanical strain and for nuclear positioning. Our work has recently demonstrated that mutations in the SUN family of proteins are associated with muscular dystrophy, resulting in defective nuclear-microtubule coupling and impaired myonuclear positioning, which is likely to contribute to muscle dysfunction in affected patients.
CABD Seminar February 19 @ noon
Of mice and cattle: evolutionary plasticity of the mechanisms that shape the vertebrate limb
Dr.Javier López Ríos
Departament of Biomedicine, University of Basel, Switzerland
CABD Seminar February 10 @ noon
How cell fusion sculpts organs
Dr. Benjamin Podbilewicz
Technion - Israel Institute of Technology
CABD Seminar February 6 @ noon
Decoding wiring specificity in the fly visual system
Dr. Marta Morey
Departament de Genètica, Facultat de Biologia, Universitat de Barcelona

Summary: How neurons select their synaptic partners and form specific connections has been a longstanding question in neurobiology. Our hypothesis is that molecular differences between closely related neurons with distinct wiring specificity would generate their unique connectivity patterns. Thus, we have profiled the transcriptomes of two classes of Drosophila photoreceptor neurons, R7 and R8, and all lamina neurons (L1-L5). These neurons elaborate distinct patterns of connections in the medulla, a multilayered neuropil of the optic lobe. Several hundred genes appear differentially expressed between these neurons in pairwise comparisons. Cell surface molecules appeared enriched among the differentially expressed genes, consistent with their role as final effectors in cell-cell interactions. Through co-expression network analysis we have found distinct networks for each type of neuron. In these networks a few transcription factors co-clustered with an array of CSM among other types of genes. These findings outline the genetic programs linking wiring specificity effectors to cell type specific transcriptional regulatory programs. Using genetic and molecular approaches we are addressing the role of these genes in wiring specificity.
CABD Seminar January 16 @ noon
Role of the gut microbiome in complications of a human developmental disorder
Dr. Naomi Ward
Department of Molecular Biology, University of Wyoming

Summary: The intestinal microbiome comprises a vast population of microbes essential for the maintenance of intestinal homeostasis, including regulation of gut development, mucosal inflammation, intestinal immunity, and barrier integrity. Given the importance of the microbiome in human health, understanding the factors determining its composition and diversity is essential. Many of these factors are external, including mode of delivery at birth, diet, and antibiotic usage, but microbiome composition is also regulated by intrinsic host factors. This host–microbial interdependence has been implicated in the etiopathogenesis of multiple gastrointestinal disorders, as well as obesity and metabolic syndrome. Hirschsprung’s disease (HD) features terminal aganglionosis of the colon, resulting from the failure of neural crest-derived cells to form the distal enteric nervous system. The most serious complication is Hirschsprung’s-associated enterocolitis (HAEC), an inflammatory colitis that can lead to bacterial translocation, sepsis, and death. Its etiology is unknown, but abnormalities in epithelial barrier function, mucosal immunity, and the microbiome have been proposed. We used 16S ribosomal RNA gene pyrosequencing to characterize the colonic microbiota in a mouse model of Hirschsprung’s disease. Our results showed early and sustained disruption of normal microbiome composition, indicating an important role for the ENS in establishment and maturation of the microbiome, and supporting our hypothesis that the microbiome may contribute to HAEC. Next steps in this research include fecal transfer experiments into germ-free mice, as well as longitudinal microbiota surveys in human HD patients.

2014 seminars

2013 seminars

2012 seminars

2011 seminars

2010 seminars

2009 seminars