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43
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April 2013 - August 2014
September 2008 - March 2013
September 2014 - present
Publications
Publications (43)
Cell shape is determined by cellular mechanics. Cell deformations in animal cells, such as those required for cell migration, division or epithelial morphogenesis, are largely controlled by changes in mechanical stress and tension at the cell surface. The plasma membrane and the actomyosin cortex control surface mechanics and determine cell surface...
Animal cell shape is controlled primarily by the actomyosin cortex, a thin cytoskeletal network that lies directly beneath the plasma membrane. The cortex regulates cell morphology by controlling cellular mechanical properties, which are determined by network structure and geometry. In particular, cortex thickness is expected to influence cell mech...
Single cells and multicellular tissues rapidly heal wounds. These processes are considered distinct, but one mode of healing--Rho GTPase-dependent formation and closure of a purse string of actin filaments (F-actin) and myosin-2 around wounds--occurs in single cells and in epithelia. Here, we show that wounding of one cell in Xenopus embryos elicit...
Integrin-dependent cell-extracellular matrix adhesion is essential for wound healing, embryonic development, immunity, and tissue organization. Here, we present a protocol for the imaging and quantitative analysis of integrin-dependent cell-matrix adhesions. We describe steps for cell culture; virus preparation; lentiviral transduction; imaging wit...
Epithelial tissues are crucial to maintaining healthy organization and compartmentalization in various organs and act as a first line of defense against infection in barrier organs such as the skin, lungs and intestine. Disruption or injury to these barriers can lead to infiltration of resident or foreign microbes, initiating local inflammation. On...
Metastasis is a hallmark of cancer and the leading cause of mortality among cancer patients. Cancer, in its most deadly form, is thus not only a disease of uncontrolled cell growth but also a disease of uncontrolled cell migration. The study of tumor cell migration requires both experimental systems that are representative of the complex tumor envi...
Collective cell migration on extracellular matrix (ECM) networks is a key biological process involved in development, tissue homeostasis and diseases such as metastatic cancer. During invasion of epithelial cancers, cell clusters migrate through the surrounding stroma, which is comprised primarily of networks of collagen-I fibers. There is growing...
Cell competition refers to the mechanism whereby less fit cells (“losers”) are sensed and eliminated by more fit neighboring cells (“winners”) and arises during many processes including intracellular bacterial infection. Extracellular matrix (ECM) stiffness can regulate important cellular functions, such as motility, by modulating the physical forc...
Growing evidence suggests that the physical properties of the cellular microenvironment influence cell migration. However, it is not currently understood how active physical remodelling by cells affects migration dynamics. Here we report that cell clusters seeded on deformable collagen-I networks display persistent collective migration despite not...
Actomyosin contractility is a major engine of preimplantation morphogenesis, which starts at the 8-cell stage during mouse embryonic development. Contractility becomes first visible with the appearance of periodic cortical waves of contraction (PeCoWaCo), which travel around blastomeres in an oscillatory fashion. How contractility of the mouse embr...
In animal cells, shape is mostly determined by the actomyosin cortex, a thin cytoskeletal network underlying the plasma membrane. Myosin motors generate tension in the cortex, and tension gradients result in cellular deformations. As such, many cell morphogenesis studies have focused on the mechanisms controlling myosin activity and recruitment to...
Intestinal organoids capture essential features of the intestinal epithelium such as crypt folding, cellular compartmentalization and collective movements. Each of these processes and their coordination require patterned forces that are at present unknown. Here we map three-dimensional cellular forces in mouse intestinal organoids grown on soft hyd...
Collective migration is a crucial process for tissue morphogenesis during development, homeostasis in adult organs, and cancer metastasis. Collective cell migration relies on the coordination of an active cell migration machinery, cell–substrate interactions, and cell–cell adhesion. The mechanical and dynamical properties of each of these elements...
There is growing evidence that the physical properties of the cellular environment can impact cell migration. However, it is not currently understood how active physical remodeling of the network by cells affects their migration dynamics. Here, we study collective migration of small clusters of cells on deformable collagen-1 networks. Combining the...
In the early stages of metastasis, cancer cells exit the primary tumor and enter the vasculature. Although most studies have focused on the tumor invasive front, cancer cells from the tumor core can also potentially metastasize. To address cell motility in the tumor core, we imaged tumor explants from spontaneously forming tumors in mice in real ti...
Screening of small molecule libraries offers the potential to identify compounds that inhibit specific biological processes and, ultimately, to identify macromolecules that are important players in such processes. To date, however, most screens of small molecule libraries have focused on identification of compounds that inhibit known proteins or pa...
Chemotaxis is an important biological process involved in the development of multicellular organisms, immune response and cancer metastasis. In order to better understand how cells follow chemical cues in their native environments, we recently developed a microfluidics-based chemotaxis device that allows for observation of cells or cell aggregates...
In many cell types, migration can be oriented towards a chemical stimulus. In mammals, for example, embryonic cells migrate to follow developmental cues, immune cells migrate toward sites of inflammation, and cancer cells migrate away from the primary tumour and toward blood vessels during metastasis. Understanding how cells migrate in 3D environme...
Cancer-associated fibroblasts (CAFs) are the most abundant cells of the tumor stroma. Their capacity to contract the matrix and induce invasion of cancer cells has been well documented. However, it is not clear whether CAFs remodel the matrix by other means, such as degradation, matrix deposition, or stiffening. We now show that CAFs assemble fibro...
Animal cell shape is largely determined by the cortex, a thin actin network underlying the plasma membrane in which myosin-driven stresses generate contractile tension. Tension gradients result in local contractions and drive cell deformations. Previous cortical tension regulation studies have focused on myosin motors. Here, we show that cortical a...
Cell shape regulation is key to a number of fundamental biological processes, including cell migration and division. In animal cells, cell morphology is controlled primarily by the cortex, a thin actomyosin network underlying the plasma membrane. The cortex determines global physical properties of the cell, such as tension. Previous studies have sh...
Metastasis begins with the invasion of tumor cells into the stroma and migration toward the blood stream. Human pathology studies suggest that tumor cells invade collectively as strands, cords and clusters of cells into the stroma, which is dramatically reorganized during cancer progression. Cancer cells in intravital mouse models and in vitro disp...
Screening of small molecule libraries offers the potential to identify compounds that inhibit specific biological processes and, ultimately, to identify macromolecules that are important players in such processes. To date, however, most screens of small molecule libraries have focused on identification of compounds that inhibit known proteins or pa...
Many cell types undergo dramatic changes in shape throughout the cell cycle. For individual cells, a tight control of cell shape is crucial during cell division, but also in interphase, for example during cell migration. Moreover, cell cycle-related cell shape changes have been shown to be important for tissue morphogenesis in a number of developme...
Cellular damage triggers rapid resealing of the plasma membrane and repair of the cortical cytoskeleton. Plasma membrane resealing results from calcium-dependent fusion of membranous organelles and the plasma membrane at the site of the damage. Cortical cytoskeletal repair results from local assembly of actin filaments (F-actin), myosin-2 and micro...
Questions
Questions (2)
We are designing a strategy to make CRISPR knock-in intestinal organoids using Lentiviral delivery (as other transfection method are very inefficient in intestinal organoids). For designing the guide RNA, this seems straightforward, and we are planning to use the lentiCRISPRv2. However, for the repair template we are struggling to figure out which backbone would be best. The worry is that cloning our repair template with homology arms into a constitutive Lenti plasmid would result in random insertions of the homology arms and tag instead of being used as a repair template. Does anyone have experience doing CRISPR knock-ins using lentiviral delivery that might be able to give some advice? Thanks!
Hello Research Gate Community!
I am teaching a class on immunology for a general cell biology course, pretty much following the immunology chapter in Alberts (chapter 24). I was confused about a figure think I may have found a mistake in figure 24-47 but wanted to check with the community since my immunology background is not particularly strong. In the attached figure 24-47, on the right it shows antigen presentation between the effector-T-cell and B-cell. As I understand it, and as described in the legend, B cells bind antigen via their BCR, internalize and proteolyze it and and present it on MHC class II, which is recognized by the TCR on the T-cell. In the picture, I think the TCR-Antigen-MHC-II complex is upside down. The TCR (in black) should be down, attached to the T-Cell, right? And the MHC-II (green) should be above, on the B-Cell, right? I want to make sure I understand the process well for the class and would also report this mistake to the publishers. Thanks for your help!
