staff

Madlaina Kuby Boillat

Postdoctoral fellow in Neurogenetics

  • T: +41 22 379 32 82
  • office 4041 (Sciences III)
  • Transcriptional adaptation of olfactory sensory neurons to GPCR identity and activity. Nat Commun 2022 May;13(1):2929. 10.1038/s41467-022-30511-4. 10.1038/s41467-022-30511-4.

    abstract

    In mammals, chemoperception relies on a diverse set of neuronal sensors able to detect chemicals present in the environment, and to adapt to various levels of stimulation. The contribution of endogenous and external factors to these neuronal identities remains to be determined. Taking advantage of the parallel coding lines present in the olfactory system, we explored the potential variations of neuronal identities before and after olfactory experience. We found that at rest, the transcriptomic profiles of mouse olfactory sensory neuron populations are already divergent, specific to the olfactory receptor they express, and are associated with the sequence of these latter. These divergent profiles further evolve in response to the environment, as odorant exposure leads to reprogramming via the modulation of transcription. These findings highlight a broad range of sensory neuron identities that are present at rest and that adapt to the experience of the individual, thus adding to the complexity and flexibility of sensory coding.

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  • From immune to olfactory expression: neofunctionalization of formyl peptide receptors. Cell Tissue Res 2021 Jan;():. 10.1007/s00441-020-03393-5. 10.1007/s00441-020-03393-5.

    abstract

    Variations in gene expression patterns represent a powerful source of evolutionary innovation. In a rodent living about 70 million years ago, a genomic accident led an immune formyl peptide receptor (FPR) gene to hijack a vomeronasal receptor regulatory sequence. This gene shuffling event forced an immune pathogen sensor to transition into an olfactory chemoreceptor, which thus moved from sensing the internal world to probing the outside world. We here discuss the evolution of the FPR gene family, the events that led to their neofunctionalization in the vomeronasal organ and the functions of immune and vomeronasal FPRs.

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  • SARS-CoV-2 receptors and entry genes are expressed in the human olfactory neuroepithelium and brain. iScience 2020 Nov;():101839. 10.1016/j.isci.2020.101839. S2589-0042(20)31036-1. PMC7685946.

    abstract

    Reports indicate an association between COVID-19 and anosmia, as well as the presence of SARS-CoV-2 virions in the olfactory bulb. To test whether the olfactory neuroepithelium may represent a target of the virus, we generated RNA-seq libraries from human olfactory neuroepithelia, in which we found substantial expression of the genes coding for the virus receptor angiotensin-converting enzyme-2 (ACE2), and for the virus internalization enhancer TMPRSS2. We analyzed a human olfactory single-cell RNA-seq dataset and determined that sustentacular cells, which maintain the integrity of olfactory sensory neurons, express and . ACE2 protein was highly expressed in a subset of sustentacular cells in human and mouse olfactory tissues. Finally, we found transcripts in specific brain cell types, both in mice and humans. Sustentacular cells thus represent a potential entry door for SARS-CoV-2 in a neuronal sensory system that is in direct connection with the brain.

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  • Neuroinflammation-Associated Aspecific Manipulation of Mouse Predator Fear by Toxoplasma gondii. Cell Rep 2020 Jan;30(2):320-334.e6. S2211-1247(19)31669-9. 10.1016/j.celrep.2019.12.019.

    abstract

    In rodents, the decrease of felid aversion induced by Toxoplasma gondii, a phenomenon termed fatal attraction, is interpreted as an adaptive manipulation by the neurotropic protozoan parasite. With the aim of understanding how the parasite induces such specific behavioral modifications, we performed a multiparametric analysis of T. gondii-induced changes on host behavior, physiology, and brain transcriptome as well as parasite cyst load and distribution. Using a set of complementary behavioral tests, we provide strong evidence that T. gondii lowers general anxiety in infected mice, increases explorative behaviors, and surprisingly alters predator aversion without selectivity toward felids. Furthermore, we show a positive correlation between the severity of the behavioral alterations and the cyst load, which indirectly reflects the level of inflammation during brain colonization. Taken together, these findings refute the myth of a selective loss of cat fear in T. gondii-infected mice and point toward widespread immune-related alterations of behaviors.

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  • The vomeronasal system mediates sick conspecific avoidance. Curr. Biol. 2015 Jan;25(2):251-5. S0960-9822(14)01555-3. 10.1016/j.cub.2014.11.061.

    abstract

    Although sociability offers many advantages, a major drawback is the increased risk of exposure to contagious pathogens, like parasites, viruses, or bacteria. Social species have evolved various behavioral strategies reducing the probability of pathogen exposure. In rodents, sick conspecific avoidance can be induced by olfactory cues emitted by parasitized or infected conspecifics. The neural circuits involved in this behavior remain largely unknown. We observed that olfactory cues present in bodily products of mice in an acute inflammatory state or infected with a viral pathogen are aversive to conspecifics. We found that these chemical signals trigger neural activity in the vomeronasal system, an olfactory subsystem controlling various innate behaviors. Supporting the functional relevance of these observations, we show that preference toward healthy individuals is abolished in mice with impaired vomeronasal function. These findings reveal a novel function played by the vomeronasal system.

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