Integrated Calendar

Relationships between gut microbial ecosystems and their vertebrate hosts have been shown in recent years to play an essential role in the well-being and proper function of their hosts. In my lecture, I will discuss some of our recent findings regarding such ecosystems stability, development, and interaction with the host.

To communicate and work cooperatively, organelles must come into close proximity at membrane contact sites to transfer lipids and small metabolites. Despite our increasing understanding of membrane contact sites, many of their molecular components have yet to be identified, making it difficult to investigate their over-arching roles in cellular and organism function. To overcome this limitation, we established a systematic and high throughput microscopy approach to identify contact site resident proteins in the budding yeast Saccharomyces cerevisiae. Using this method, we have identified multiple new contact site proteins. I will share an example of how mechanistic follow-up on such new contact residents is leading to a new understanding of organelle Biology.

The sinking of organic particles in the ocean and their degradation by marine microorganisms drive one of the most conspicuous carbon fluxes on Earth, the biological pump. Yet, the mechanisms determining the magnitude of the pump remain poorly understood, limiting our ability to predict this carbon flux in future ocean scenarios. Current ocean models assume that the biological pump is governed by the competition between sinking speed and degradation rate, with the two processes independent from one another. In this talk, I will demonstrate that contrary to this paradigm, sinking itself is a primary determinant of the rate at which bacteria enzymatically degrade particles in the ocean. By combining video microscopy and microfluidic experiments to directly observe and quantify bacterial degradation of individual organic particles in flow, I will show that even modest sinking speeds of 8 meters per day enhance degradation rates more than 10-fold. I will further discuss the molecular mechanism behind the sinking-enhanced degradation, as well as possible ways by which bacteria can slow the sinking of particles. Finally, using the results obtained from a mathematical model, I will show that the coupling of sinking and degradation may contribute to determining the magnitude of the vertical carbon flux in the ocean, and will outline major open questions in the field.

Nonoscillatory coding and multiscale representation of very large environments in the bat hippocampus

Abstract: The hippocampus plays a key role in memory and navigation, and forms a cognitive map of the world: hippocampal ‘place cells’ encode the animal’s location by activating whenever the animal passes a particular region in the environment (the neuron’s ‘place field’). Over the last 50 years of hippocampal research, almost all studies have focused on rodents as animal models, using small laboratory experimental setups. In my research, I explored hippocampal representations in a naturalistic settings, in a unique animal model – the bat. My talk will outline two main stories: (i) In rodents, hippocampal activity exhibits ‘theta oscillations’. These oscillations were proposed to support multiple functions, including memory and sequence formation. However, absence of clear theta in bats and humans has questioned these proposals. Surprisingly, we found that in bats hippocampal neurons exhibited nonoscillatory phase-coding. This highlights the importance of phase-coding, but not oscillations per se, for hippocampal function across species – including humans. (ii) Real-world navigation requires spatial representation of very large environments. To investigate this, we wirelessly recorded from hippocampal dorsal CA1 neurons of bats flying in a long tunnel (200 meters). Place cells displayed a multifield multiscale code: Individual neurons exhibited multiple place fields of diverse sizes, ranging from 0.6 to 32 meters, and the fields of the same neuron differed up to 20-fold in size. Theoretical analysis showed that the multiscale code allows representing large environments with much better accuracy than other codes. Thus, by increasing the spatial scale, we uncovered a neural code that is radically different from classical spatial codes. Together, these results highlight the power of the comparative approach, and demonstrate that studying the brain under naturalistic settings and behavior enables discovering new unknown aspects of the neural code.

There is Chemistry in Social Chemistry
Abstract: Non-human terrestrial mammals constantly sniff themselves and each-other, and based on this decide who is friend or foe. Humans also constantly sniff themselves and each-other, but the functional significance of this behavior is unknown. Given that humans seek friends who are similar to themselves, we hypothesized that humans may be smelling themselves and others to subconsciously estimate body-odor similarity, and that this may then promote friendship. To test this hypothesis, we recruited non-romantic same-sex friend dyads who had initially bonded instantaneously, or so called click-friends, and harvested their body-odor. In a series of experiments, we then found that objective ratings obtained with an electronic nose, and subjective ratings obtained from independent human smellers, converged to suggest that click-friends smell more similar to each other than random dyads. To then estimate whether this similarity was merely a consequence of friendship, or a driving force of friendship, we recruited complete strangers, smelled them with an electronic nose, and engaged them in non-verbal same-sex dyadic interactions. Remarkably, we observed that dyads who smelled more similar had better dyadic interactions. In other words, we could predict social bonding with an electronic nose. This result implies that body-odor similarity is a causal factor in social interaction, or in other words, there is indeed chemistry in social chemistry.

Chromosomal instability is one of the major hallmarks in cancer driving numerical and structural chromosome aberrations. Cancer cells can use the chaotic background of chromosome instability to generate ordered genomic events leading to accelerated tumor formation or drug resistance. I will show how chromothripsis, the catastrophic shattering of a chromosome and random religation of its pieces, can promote resistance to therapy. Using cancer cells and patient samples, I identified that chromothripsis drives the formation and evolution of extrachromosomal DNA (ecDNA) elements that can amplify genes conferring drug resistance. I will then discuss how transient centrosome amplification can induce a burst of chromosomal instability in vivo. This triggers the formation of random aneuploidies (changes in chromosome numbers) with cancer initiating cells carrying a specific aneuploidy signature leading to accelerated tumorigenesis. This work has uncovered aneuploidy as a direct driver of cancer and enables a better understanding of the involvement of specific aneuploidies in cancer.