Biology subjects

de Seze, J.

Publications and source records attributed to de Seze, J..

3 recordsLinked to original sources

bioRxiv2023

Setting a trajectory for CO2 emission reduction in academic research: a case study of a French biophysics laboratory

Climate change is a scientifically proven phenomenon caused by anthropic activities, which requires urgent and significant reductions in greenhouse gas emissions. Despite the increasing vocalization of scientists advocating for political action, the issue of the environmental impact of academic research has been neglected for some time. Now, field-dependent initiatives have emerged, such as the non-profit organization My Green Lab, which delivers green certifications to biology and chemistry labs, and institute-dependent programs, such as the Max Planck Sustainability Network. In France, an independent collective was founded in 2019 to address the environmental footprint of academic research following the COP 15 Paris Agreement: Labos 1Point5. Building on their resources and methodology, we have quantified the overall carbon footprint of our biophysics laboratory, considering energy consumption, purchases and travel, for the year 2021. We investigate how this footprint would decrease by 2030 following systemic changes (change in the energy mix, improvements from suppliers), and we propose scenarios based on additional voluntary initiatives to reach a final reduction of -50% compared to the 2021 baseline, following IPCC targets. We have now formed a group of more than 20 colleagues to achieve this goal, emphasizing the importance of collective action. Finally, we provide advice based on our own experience to assist others in addressing the environmental impact of academic research in their respective laboratories.

scientific communication and education↗

bioRxiv2023

Control of cell retraction and protrusion with a single protein

The ability of a single protein to trigger different functions is an assumed key feature of cell signaling, yet there are very few examples demonstrating it. Here, using an optogenetic tool to control membrane localization of RhoA nucleotide exchange factors (GEFs), we present a case where the same protein can trigger both protrusion and retraction when recruited to the plasma membrane, polarizing the cell in two opposite directions. We show that the basal concentration of the GEF prior to activation predicts the resulting phenotype. A low concentration leads to retraction, whereas a high concentration triggers protrusion. This unexpected protruding behavior arises from the simultaneous activation of Cdc42 by the GEF and sequestration of active RhoA by the GEF PH domain at high concentrations. We propose a minimal model that recapitulates the phenotypic switch, and we use its predictions to control the two phenotypes within selected cells by adjusting the frequency of light pulses. Our work exemplifies a unique case of control of antagonist phenotypes by a single protein that switches its function based on its concentration or dynamics of activity. It raises numerous open questions about the link between signaling protein and function, particularly in contexts where proteins are highly overexpressed, as often observed in cancer.

cell biology↗

bioRxiv2020

Cell clusters adopt a collective amoeboid mode of migration in confined non-adhesive environments

Cell migration is essential to most living organisms. Single cell migration involves two distinct mechanisms, either a focal adhesion- and traction-dependent mesenchymal motility or an adhesion-independent but contractility-driven propulsive amoeboid locomotion. Cohesive migration of a group of cells, also called collective cell migration, has been only described as an adhesion- and traction-dependent mode of locomotion where the driving forces are mostly exerted at the front by leader cells. Here, by studying primary cancer specimens and cell lines from colorectal cancer, we demonstrate the existence of a second mode of collective migration which does not require adhesion to the surroundings and relies on a polarised supracellular contractility. Cell clusters confined into non-adhesive microchannels migrate in a rounded morphology, independently of the formation of focal adhesions or protruding leader cells, and lacking internal flow of cells, ruling-out classical traction-driven collective migration. Like single cells migrating in an amoeboid fashion, the clusters display a supracellular actin cortex with myosin II enriched at the rear. Using pharmacological inhibitors and optogenetics, we show that this polarised actomyosin activity powers migration and propels the clusters. This new mode of migration, that we named collective amoeboid, could be enabled by intrinsic or extrinsic neoplasic features to enable the metastatic spread of cancers. One Sentence SummaryClusters organise as polarised and contractile super-cells to migrate without adhesion.

cell biology↗