I pursued a PhD in Biomedicine in the Cell Cycle group directed by Dr. Ethel Queralt at the Cancer Biology and Epigenetics Department, in Barcelona (Spain). During my PhD, I made fundamental discoveries in the role of mitotic exit pathways in regulating proper chromosome segregation and cytokinesis in the well established model organism S. cerevisae. After my PhD, I decided to pursue a one-year postdoctoral opportunity focused on Plasmodium vivax malaria, which is considered a “neglected” human disease. I moved to the Tropical Medicine Foundation in Manaus (Amazonas, Brazil), where I worked in close collaboration with the Global Health Institute in Barcelona (Spain) as part of the Brazilian Science Without Borders Program. Under the supervision of Dr. Marcus Lacerda and Dr. Hernando del Portillo, I investigated the molecular causes of anemia in patients with Plasmodium vivax malaria. The project involved molecular analyses of bone marrow samples from malaria-infected patients. After my year in Brazil, I decided to pursue a postdoctoral fellowship that will enable me to learn the state-of-the-art molecular techniques applied to malaria research. I recently joined Dr. Elizabeth Egan’s laboratory at Stanford University, where I will build on my experiences in cell cycle research and malaria biology. For my research in the Egan lab I plan to focus on identifying and characterizing key molecular events that control the parasite cell cycle, with a particular focus on host factors that influence these events. The long-term goal of my research is to identify potential targets for new types of therapeutics to treat or prevent malaria.

Academic Appointments

Honors & Awards

  • Postdoctoral fellowship, Research Support Foundation of the State of Amazonia (FAPEAM, Brazil) (2014)
  • Introduction to Next Generation Sequencing, Wellcome Trust Genome Campus EMBL-EBI (England) (2014)
  • FPU fellowship (PhD students and university trainees), Spanish government (2010)
  • University exchange fellowship, ERASMUS (2007)

Research & Scholarship

Current Research and Scholarly Interests

Malaria is a mosquito-borne infectious disease caused by Plasmodium parasites that leads to enormous childhood morbidity and mortality in the developing world. Sub-Saharan Africa, where Plasmodium falciparum is the most prevalent species, carries nearly 90% of global malaria cases and deaths. A major threat to public health, malaria constrains wealth and economic development of endemic countries, as it is currently known to be both a disease of poverty and a cause of poverty.
Major efforts towards malaria control and elimination have reduced global malaria mortality and incidence during the past decade. Nevertheless, the malaria burden is still formidable (200 million cases annually) and rapid development of parasite resistance to available antimalarials is an ongoing challenge to public health. Thus, development of new drugs for malaria treatment is urgently needed.
All of the current antimalarials available target essential parasite proteins. An alternative strategy could be to target host factors required for parasite survival, a therapeutic approach that has proved promising for other challenging infectious diseases, such as HIV. However, our current understanding of host-pathogen interactions in malaria is still very limited, in part because red blood cells (where P. falciparum replicates) do not have nucleus or DNA, making genetic studies impossible.
My current research aims to surmount this roadblock by developing a state-of-the-art CRISPR-Cas9-based genetic approach using hematopoietic stem cells to explore the host’s role in malaria infection. Since hematopoietic stem cells contain a nucleus and genome, this approach allows us to perform genetic modification and then differentiate the stem cells to mature, mutant red blood cells (RBCs). I hypothesize that there are multiple host genes that influence the ability of parasites to grow and develop within RBCs, the discovery of which could lead to the development of host-directed therapeutics for malaria. I will perform a forward-genetic screen of the erythrocyte proteome to identify candidate host factors that either enhance or restrict cell cycle progression of P. falciparum in human red blood cells. In addition, I will use reverse genetics, biochemical and cell biological approaches to validate specific candidate host factors and characterize their function during parasite infection.
Uncovering essential host-parasite interactions during the malaria cell cycle will lay the foundation for a new approach to treating malaria focused on targeting critical host molecules, which could pave the way towards eradication of this deadly disease.


All Publications

  • Dual Regulation of the Mitotic Exit Network (MEN) by PP2A-Cdc55 Phosphatase PLOS GENETICS Baro, B., Rodriguez-Rodriguez, J., Calabria, I., Luisa Hernaez, M., Gil, C., Queralt, E. 2013; 9 (12)


    Exit from mitosis in budding yeast is triggered by activation of the key mitotic phosphatase Cdc14. At anaphase onset, the protease separase and Zds1 promote the downregulation of PP2A(Cdc55) phosphatase, which facilitates Cdk1-dependent phosphorylation of Net1 and provides the first wave of Cdc14 activity. Once Cdk1 activity starts to decline, the mitotic exit network (MEN) is activated to achieve full Cdc14 activation. Here we describe how the PP2A(Cdc55) phosphatase could act as a functional link between FEAR and MEN due to its action on Bfa1 and Mob1. We demonstrate that PP2A(Cdc55) regulates MEN activation by facilitating Cdc5- and Cdk1-dependent phosphorylation of Bfa1 and Mob1, respectively. Downregulation of PP2A(Cdc55) initiates MEN activity up to Cdc15 by Bfa1 inactivation. Surprisingly, the premature Bfa1 inactivation observed does not entail premature MEN activation, since an additional Cdk1-Clb2 inhibitory signal acting towards Dbf2-Mob1 activity restrains MEN activity until anaphase. In conclusion, we propose a clear picture of how PP2A(Cdc55) functions affect the regulation of various MEN components, contributing to mitotic exit.

    View details for DOI 10.1371/journal.pgen.1003966

    View details for Web of Science ID 000330533300014

    View details for PubMedID 24339788

  • Zds1 regulates PP2A(Cdc55) activity and Cdc14 activation during mitotic exit through its Zds_C motif JOURNAL OF CELL SCIENCE Calabria, I., Baro, B., Rodriguez-Rodriguez, J., Russinol, N., Queralt, E. 2012; 125 (12): 2875-2884


    At anaphase onset, highly active mitotic cyclin-dependent kinase (Cdk) is inactivated to promote exit from mitosis and completion of cytokinesis. The budding yeast Cdc14p phosphatase is a key mitotic regulator that counteracts cyclin-dependent kinase (Cdk) activity during mitotic exit. Separase, together with Zds1p, promotes the downregulation of the protein phosphatase 2A in conjunction with its Cdc55p regulatory subunit (PP2A(Cdc55)) in early anaphase, enabling accumulation of phosphorylated forms of Net1p and release of Cdc14p from the nucleolus. Here we show that the C-terminal domain of Zds1p, called the Zds_C motif, is required for Zds1-induced release of Cdc14p, and the N-terminal domain of the protein might be involved in regulating this activity. More interestingly, Zds1p physically interacts with Cdc55p, and regulates its localization through the Zds_C motif. Nevertheless, expression of the Zds_C motif at endogenous levels cannot induce timely release of Cdc14p from the nucleolus, despite the proper (nucleolar) localization of Cdc55p. Our results suggest that the activity of PP2A(Cdc55) cannot be modulated solely through regulation of its localization, and that an additional regulatory step is probably required. These results suggest that Zds1p recruits PP2A(Cdc55) to the nucleolus and induces its inactivation by an unknown mechanism.

    View details for DOI 10.1242/jcs.097865

    View details for Web of Science ID 000307767100011

    View details for PubMedID 22427694