Biology subjects

Faure, L. M.

Publications and source records attributed to Faure, L. M..

5 recordsLinked to original sources

bioRxiv2024

Fine Social Discrimination of Siblings in Mice: Implications for Early Detection of Alzheimer's Disease

The ability to distinguish between individuals is crucial for social species and supports behaviors such as reproduction, hierarchy formation, and cooperation. In rodents, social discrimination relies on memory and the recognition of individual-specific cues, known as "individual signatures". While olfactory signals are central, other sensory cues --such as auditory, visual, and tactile inputs -- also play a role. However, little research has explored the fine discrimination of individuals with overlapping cues, such as siblings or cohabitating mice. This study investigates whether mice can discriminate between two closely related individuals: siblings from the same litter and cage. We tested the hypothesis that it would be more challenging for mice to distinguish between siblings than between unrelated mice due to shared cues. Moreover, social cognitive impairments are common in neurodegenerative diseases like Alzheimers disease (AD), where difficulties in recognizing faces and voices progressively disrupt social interactions in patients. Using a mouse model of AD (Tg2576), known for the progressive onset of cognitive deficits, we assessed whether the ability to discriminate between siblings is preserved in "pre-symptomatic" animals. Thus, we first demonstrated that male and female C57BL6/J mice can discriminate siblings, regardless of sex. Next, we revealed that "pre-symptomatic" 3-month-old Tg2576 mice exhibit impairments in fine social memory, while their general social memory remains unaffected. Thus, we demonstrate that the inability to perform fine social discrimination is an early cognitive impairment that arises before other well-documented memory abnormalities in this AD mouse model. SIGNIFICANCE STATEMENTDiscriminating between individuals is vital for social species, supporting reproduction, hierarchy formation and cooperation. This study examined whether mice can perform fine social discrimination, i.e., distinguish between siblings from the same home cage. We found that both male and female C57BL6/J mice can discriminate siblings, regardless of their sex. Notably, this fine social discrimination ability is impaired in mouse model of Alzheimers disease (AD) at a very early stage of the pathology, i.e., at an age when they can still recognize two unrelated mice from different home cages. This suggests that fine social discrimination deficits occur early in AD, and could serve as an early marker of the pathology.

animal behavior and cognition↗

bioRxiv2024

3D micropatterned traction force microscopy: a technique to control three-dimensional cell shape while measuring cell-substrate force transmission.

Cell shape and function are intimately linked, in a way that is mediated by the forces exerted between cells and their environment. The relationship between cell shape and forces has been extensively studied for cells seeded on flat 2-dimensional (2D) substrates, but not for cells in more physiological three-dimensional (3D) settings. Here, we demonstrate a technique called 3D micropatterned traction force microscopy (3D-TFM) to confine cells in three-dimensional wells of defined shape, while simultaneously measuring the forces transmitted between cells and their microenvironment. This technique is based on the 3D micropatterning of polyacrylamide wells and on the calculation of 3D traction force from their deformation. With 3D-TFM, we show that MCF10A breast epithelial cells exert defined, reproducible patterns of forces on their microenvironment, which can be both contractile and extensile. We further show that cells switch from a global contractile to extensile behaviour as their volume is reduced. Our technique enables the quantitative study of cell mechanobiology with full access to 3D cellular forces while having accurate control over cell morphology and the mechanical conditions of the microenvironment.

bioengineering↗

bioRxiv2023

Integrin-like adhesin CglD confers traction and stabilizes bacterial focal adhesions involved in myxobacterial gliding motility

AO_SCPLOWBSTRACTC_SCPLOWIntegrins are crucial for eukaryotic cell attachment and motility within the extracellular matrix (ECM) via focal-adhesion formation, with their evolutionary emergence important for the development of multicellularity. Intriguingly, single gliding cells of the predatory deltaproteobacterium Myxococcus xanthus form bacterial focal-adhesion (bFA) sites; therein, helically-trafficked motors become immobilized at anchored locations through Glt apparatus association with cell-surface integrin I-domain-like adhesin CglB. Using traction-force, bead-force, and total internal reflection-fluorescence microscopies combined with biochemical approaches, we herein identify the von Willebrand A domain-containing cell-surface lipoprotein CglD to be a {beta}-integrin-like outer-membrane lipoprotein that functionally associates with and anchors the trans-envelope Glt-CglB gliding apparatus, stabilizing and efficiently anchoring this assembly at bFAs. Calcium dependence governs CglD importance, consistent with its integrated ECM eukaryotic cartilage oligomeric matrix protein domains. CglD thus confers mechanosensory and mechanotransductory capabilities to the gliding apparatus, helping explain bFA-mediated trans-envelope force transduction, from inner-membrane-embedded motors to the cell surface.

microbiology↗

bioRxiv2021

Competition for endothelial cell polarity drives vascular morphogenesis

Blood vessel formation generates unique vascular patterns in each individual. The principles governing the apparent stochasticity of this process remain to be elucidated. Using mathematical methods, we find that the transition between two fundamental vascular morphogenetic programs - sprouting angiogenesis and vascular remodeling - is established by a shift on collective front-rear polarity of endothelial cells. We demonstrate that the competition between biochemical (VEGFA) and mechanical (blood flow-induced shear stress) cues controls this collective polarity shift. Shear stress increases tension at focal adhesions overriding VEGFA-driven collective polarization, which relies on tension at adherens junctions. We propose that vascular morphogenetic cues compete to regulate individual cell polarity and migration through tension shifts that translates into tissue-level emergent behaviors, ultimately leading to uniquely organized vascular patterns.

developmental biology↗

bioRxiv2020

CglB adhesins secreted at bacterial focal adhesions mediate gliding motility

AO_SCPLOWBSTRACTC_SCPLOWThe predatory deltaproteobacterium Myxococcus xanthus uses a helically-trafficked motor at bacterial focal adhesion (bFA) sites to power gliding motility. Using TIRF and force microscopy, we herein identify the integrin I-domain-like outer-membrane (OM) lipoprotein CglB as an essential substratum-coupling protein of the gliding motility complex. Similar to most known OM lipoproteins, CglB is anchored on the periplasmic side of the OM and thus a mechanism must exist to secrete it to the cell surface in order for it to interact with the underlying substratum. We reveal this process to be mediated by a predicted OM {beta}-barrel structure of the gliding complex. This OM platform was found to regulate the conformational activation and secretion of CglB across the OM. These data suggest that the gliding complex promotes surface exposure of CglB at bFAs, thus explaining the manner by which forces exerted by inner-membrane motors are transduced across the cell envelope to the substratum; they also uncover a novel protein secretion mechanism, highlighting the ubiquitous connection between secretion and bacterial motility.

microbiology↗