Integrated Calendar

Diatoms are among the most globally distributed and ecologically successful organisms in the modern ocean, contributing upwards of 40% of total marine primary productivity. Diatom production is tightly coupled with carbon export through the ballasted nature of the silica-based cell wall, linking the oceanic silicon and carbon cycles. While viruses are considered key players in ocean biogeochemical cycles, little is known about how viral infection specifically impacts diatom populations. Using a suite of molecular, physiological and geochemical approaches, we explored diatoms and associated viruses across diverse nutrient regimes in the northeast Pacific. We found that silicon (Si) limitation facilitated virus infection and mortality in diatoms while the onset of iron (Fe) limitation, in sharp contrast, substantially reduced viral replication. These findings, recapitulated in model systems, suggest that virus-mediated mortality in Si-limited regimes would facilitate diatom remineralization in the surface ocean, while diatoms in Fe-limited regimes may escape viral lysis, ultimately contributing to carbon export. We also explored how viral infection of diatoms might impact the microbial processing of organic matter in the ocean. Using bacterial isolates and model diatom host-virus systems, we tested how bacteria respond to dissolved organic matter generated during viral infection in diatoms. We found that this material can significantly stimulate ectoproteolytic activity, implicating viral infection of diatoms in bacteria-mediated recycling of organic matter and silica in the surface ocean. Together, these findings highlight the dynamic role that diatom host–virus interactions play in shaping the biogeochemical landscape the global ocean.

Zoom: https://weizmann.zoom.us/j/93321256211?pwd=TXNaWGw0ZjBJVGpnZUFMMFdpbElaQT09
Passcode: 379614


Crystallization plays an important role in many areas of biology, chemistry and materials science, but the underlying mechanisms that govern crystallization are still poorly understood because of experimental limitations in the analysis of such complex, evolving systems. To derive a fundamental understanding of crystallization processes, it is essential to access the sequence of solid phases produced as a function of time, with atomic-level resolution. Rationalization of crystallization processes is particularly relevant for polymorphic materials, i.e. solids that can exist as distinct crystalline forms. Indeed, polymorphism can have huge economic and practical consequences for industrial applications in pharmacy and energy because different polymorphs display different physicochemical properties. If, on the one hand, it offers great opportunities for tuning the performance of the material, on the other hand, manufacture or storage-induced, unexpected, polymorph transitions can compromise the end-use of the solid product. Interestingly, these transformations often imply the formation of metastable forms, which are receiving growing attention because they can offer new crystal forms with improved properties. Today, detection and accurate structural analysis of these – generally transient – forms remain challenging, essentially because of the present limitations in temporal and spatial resolution of the analysis, which prevents rationalization (and hence control) of crystallization processes.
In our group, we develop dynamic nuclear polarization (DNP) solid-state NMR approaches to overcome these limitations. In this contribution, I will present some of our latest results showing that cryogenic MAS NMR [1] combined with the sensitivity enhancement provided by DNP [2] can be an efficient way of monitoring the structural evolution of crystallizing solutions with atomic-scale resolution on a time scale of a few minutes. I will discuss current approaches and recent developments allowing to detect and characterize transient, metastable phases formed at the early stages of crystallization through the use of tailored DNP polarizing agents [3].
[1] P. Cerreia-Vioglio, G. Mollica, M. Juramy, C.E. Hughes, P.A. Williams, F. Ziarelli, S. Viel, P. Thureau, K.D.M. Harris, Angew. Chem. Int. Ed. 57, 6619 (2018)
[2] P. Cerreia-Vioglio, P. Thureau, M. Juramy, F. Ziarelli, S. Viel, P.A. Williams, C.E. Hughes, K.D.M. Harris, G. Mollica J. Phys. Chem. Lett. 10, 1505 (2019)
[3] M. Juramy, R. Chèvre, P. Cerreia-Vioglio, F. Ziarelli, E. Besson, S. Gastaldi, S. Viel, P. Thureau, K.D.M. Harris, G. Mollica J. Am. Chem. Soc. 143, 16, 6095 (2021)

Social interactions are essential for animals to survive, reproduce, raise their young. Over the years, my lab has attempted to decipher the unique characteristics of social recognition: what are the unique cues that trigger distinct social behaviors, what is the nature and identity of social behavior circuits, how is the function of these circuits different in males and females and how are they modulated by the animal physiological status? In this lecture, I will describe our recent progress in understanding how different parts of the brain participate in the positive and negative control of parental behavior in males and females, providing a new framework to understand the regulation of adult-infant interactions in health and disease. I will also describe how new approaches in in situ single cell transcript
omics have enabled us to uncover specific hypothalamic cell populations involved in distinct social behaviors. Finally, I will describe our most recent work uncovering how specific brain circuits are able to direct adaptive changes in behavior during sickness episodes in mice.

Host: Dr. Takashi Kawashima takashi.kawashima@weizmann.ac.il tel: 2995

Cancer cells recruit and rewire normal cells in their microenvironment to support and protect them by creating a pro-tumorigenic tumor microenvironment (TME). We lack an overarching view of how, despite being genomically stable, stromal cells in the tumor microenvironment are heterogeneously reprogrammed across time and space to promote the evolution of aggressive disease. Recent work by us and others has shown that fibroblasts in the tumor microenvironment are transcriptionally rewired to become protumorigenic cancer associated fibroblasts (CAFs). Here we hypothesize that CAFs are epigenetically modified and that these modifications lead to deregulation of signaling pathways and transcriptional circuitries that support tumorigenic growth in the neoplastic cells. We applied a sensitive method of whole genome bisulfide sequencing on a model of triple-negative breast cancer in mice to evaluate the methylome profile of CAFs compared to normal mammary fibroblasts (NMFs). We detected global changes in DNA methylation as well as distinct changes in promoter methylation between NMFs and breast CAFs in mice. These changes inversely correlated with transcriptional changes between CAFs and NMFs. We characterized potential regulators of this process, and tested their expression in CAFs in human breast cancer patients, to confirm relevance of our findings to human disease. Our findings suggest that epigenetic alterations contribute to the transcriptional rewiring of fibroblasts to CAFs. This work presents a comprehensive map of DNA-methylation in CAFs, and reveals a previously unknown facet of the dynamic plasticity of the stroma.