Where Ideas Grow

9th McBiology Symposium

23rd and 24th February 2023 | i3S, Porto, Portugal



The 9th edition of the Molecular and Cell Biology Symposium – “Science: everything, everywhere all at once” – is an event organized by the class of 2022 of the Doctoral Program in Molecular and Cell Biology. This edition is taking place on 23rd and 24th February 2023 at i3S - Institute for Research & Innovation in Health (Porto, Portugal). This symposium will bring together international speakers from the three main lines of research of i3S (Cancer, Host Interaction and Response, and Neurobiology and Neurologic Disorders), lectures, and poster sessions from PhD students. We are delighted to be back to face-to-face meetings and look forward to bringing our community together for another moment of science sharing. Well, for all of you, beware because, more than ever, there is Science... "Science: Everything Everywhere all at once."

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The symposium will be held at i3S – Instituto de Investigação e Inovação em Saúde.
Rua Alfredo Allen, 208; 4200-135 Porto, Portugal
Tel: +351 226 074 900 | Site: http://www.i3s.up.pt/ | E-mail: events@i3s.up.pt
GPS coordinates: 41º 10’ 30.008’’ N, 8º 36’ 12.488’’ W.


Organizing Committee

Alexandre Dias
Ana Castro
Ana Sofia Figueiredo
André Carvalho
Carla Santos
Cátia Ramos
Diana Meireles
Eduarda Gomes
Elias Weiler
Joana Almeida
Joana Marques
Joana Saavedra
Natália Rigos

The MCBiology PhD Program – organized by ICBAS (Institute of Biomedical Sciences Abel Salazar), FCUP (Faculty of Sciences of the University of Porto), and i3s (Institute for Research and Innovation in Health) – provides advanced practical and theoretical training in Molecular and Cellular Biology field. The program provides the necessary tools for the students to excel either in academia, or industry. The nineth edition is focused on the hallmarks of molecular and cellular biology to stimulate progress and multidisciplinary in life sciences discoveries.


23 February 2023

13:00 | Registration
i3S Main Hall
13:45 | Welcome Session

14:00 | Cell fate specification and plasticity of mammary stem cells
Silvia Fre | Group Leader of the Notch Signaling in Stem Cells and Tumors Group at Institut Curie

15:00 | Fluorinated GalNAc as a novel inhibitor of cancer-associated truncated O-glycans in gastrointestinal cancer. | Ana F Costa

15:15 | Dynein-1 ensures proper cell fate commitment by orienting the mitotic spindle in Caenorhabditis elegans hypodermis. | Cátia Carvalho

15:30 | Fast but not furious: neonatal cardiac fibroblasts as promoters of regeneration after myocardial infarction. | Rita N Gomes

15:45 | Coffee Break + Round Table 

Commercial talks

17h00 | NIMGenetics

17h10 | Dias de Sousa

17h20 | LusoPalex

17h30 | Sarstedt

17h40 | Macrogen

17h50 | Quimigen

18:00 | Closure


24 February 2023

9:15 | Welcome Session

9:30 | The role of natural competence in non-competent bacteria and in pathogenesis
Daniel López | Group Leader of the Molecular Infection Biology Group at the National Center for Biotechnology (CNB-CSIC) 

10:30 | Coffee break

11:00 | Severe Malaria: What’s liver got to do with it
Ângelo Chora | Senior Postdoctoral Researcher in the Group of Biology & Physiology of Malaria at Instituto de Medicina Molecular

12:00 | Toxic RNA and glial cell pathology: deciphering brain dysfunction in myotonic dystrophy
Mário Gomes-Pereira | Group Leader in the Myology Research Centre at INSERM 

13:00 | Lunch

14:00 | The transcription factor Foxo3 controls the homeostasis and functional heterogeneity of medullary thymic epithelial cells. | Camila Ribeiro

14:15 | Disclosing the role of meningeal immunity during Group B Streptococcus neonatal meningitis. | Inês Lorga

14:30 | Whole blood transcriptional analysis of M. tuberculosis vs M. africanum infected patients reveals the nuclear receptor pathway as a potential disease severity marker. | Marta Silva


14:45 | Investigating the cell-cycle regulation of mitochondrial function. | Ana Cláudia Leite

15:00 | How methamphetamine regulates the cytoskeleton of neurons and microglia. | Ana Filipa Terceiro

15:15 | Modulation of amyloid-β transporters by Transthyretin at the blood-cerebrospinal fluid barrier. | Tiago Gião

15:30 | Coffee Break


16:00 | Poster Session

17:30 | Award presentation

18:00 | Chill Out



Ângelo Chora
Senior Postdoctoral Researcher in the Group of Biology & Physiology of Malaria at Instituto de Medicina Molecular

Abstract: "Plasmodium, the causative agent of malaria, has a complex live cycle in the vertebrate host encompassing two distinct stages, i.e., the clinically silent liver-stage of infection where the parasite replicates within hepatocytes, and the blood-stage of infection, associated with the establishment of disease. The absence of clinical presentations during the liver stage of Plasmodium infection has cemented the perception that this phase of parasite development does not influence the ensuing pathology. We now show that the integration of signals from the two stages of parasite development dictates host survival or death. This dichotomy relies on the liver-stage-dependent activation of Vγ4+ δγ T cells, which exhibit distinct functional profiles selectively sustained by different blood stage parasite loads. Protection from severe malaria associates with increased splenic erythropoiesis and reticulocytosis in a γδ T cell, IL-17-dependent manner. Notably, pharmacological induction of splenic erythropoiesis or therapeutic adoptive transfer of erythroid precursors is sufficient to protect from severe pathology in the absence of either γδ T cells or IL-17. Our findings challenge the prevailing understanding on the mechanisms underlying the pathophysiology of malaria infections, repositioning Plasmodium liver-stage infection from a transient phase of parasite expansion into a critical contributor for the clinical outcome of infection."


Daniel López

Group Leader of the Molecular Infection Biology Group at the National Center for Biotechnology (CNB-CSIC)

Abstract: "A central question concerning natural competence is why orthologs of competence genes are conserved in non-competent bacterial species, suggesting they have a role other than in transformation. I will show that competence induction in the human pathogen Staphylococcus aureus occurs in response to ROS and host defenses that compromise bacterial respiration during infection. Bacteria cope with reduced respiration by obtaining energy through fermentation instead. Since fermentation is energetically less efficient than respiration, the energy supply must be assured by increasing the glycolytic flux. The induction of natural competence increases the rate of glycolysis in bacteria that are unable to respire via upregulation of DNA- and glucose-uptake systems. A competent-defective mutant showed no such increase in glycolysis, which negatively affects its survival in both mouse and Galleria infection models. Overall, I will discuss the possibility that natural competence foster genetic variability but also provides S. aureus with additional nutritional and metabolic possibilities, allowing it to proliferate during infection."

Mário Gomes-Pereira

Group Leader in the Myology Research Centre at INSERM 

Abstract: "Brain function relies on the complex interplay between highly specialised and ramified cell types, each with differing contributions in neurological disease. Myotonic dystrophy type 1 (DM1) is caused by the abnormal expansion of a non-coding trinucleotide DNA repeat. In addition to muscle impairment, DM1 presents debilitating cognitive impairment. While it is established that mutant RNA accumulates in the nucleus of DM1 cells and perturb the activity of key RNA-binding proteins, a major gap still exists in our understanding of how each CNS cell type drives brain pathology. We sought to investigate the impact of DM1 RNA toxicity on different brain cells, taking advantage of a unique transgenic mouse model of the disease. We found a marked deleterious effect of the DM1 mutation on glia, characterised by impaired astrocyte ramification and delayed myelination in vivo, as well as defective morphology, adhesion and migration in primary culture. Glial phenotypes were associated with a pronounced spliceopathy of cytoskeleton-related transcripts in both astrocytes and oligodendrocytes, which recreated a molecular signature of impaired differentiation in response to the repeat expansion. We suggest that RNA toxicity in glia cells affects neuronal physiology through defective neuron-glia crosstalk, contributing to the abnormal neurotransmission and synaptic plasticity reported in DM1." 

Silvia Fre
Group Leader of the Notch Signaling in Stem Cells and Tumors Group at Institut Curie

Abstract: "I will present our recent results and the new approaches we are employing to understand how tissue-specific stem cells engage in differentiation while retaining self-renewal potential and plasticity, during tissue morphogenesis. I will focus on our studies on cell fate specification in the mouse mammary gland during embryonic and pubertal branching morphogenesis, using scRNAseq and in vivo imaging techniques."


Abstract Submission

The call for abstracts will be open until the 20th of January (notification of acceptance until the 20th of January). Abstract submission for oral communications are open only for McBiology students. 

Abstracts should be structured according to the following template: 

Abstract layout >>

Abstract submission form >>


Registration is free, but mandatory.
Registration includes participation in the event and certificate.

Registration is closed. 

Registration form >>



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More information:
Events Management Unit | Rua Alfredo Allen 208 | 4200-135 Porto, Portugal
Email: events@i3s.up.pt | Tel: +351 220 408 811