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X-WR-CALNAME:Mechanobiology Institute, National University of Singapore
X-ORIGINAL-URL:https://www.mbi.nus.edu.sg
X-WR-CALDESC:Events for Mechanobiology Institute, National University of Singapore
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BEGIN:VTIMEZONE
TZID:Asia/Singapore
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TZOFFSETFROM:+0800
TZOFFSETTO:+0800
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DTSTART:20170101T000000
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BEGIN:VEVENT
DTSTART;TZID=Asia/Singapore:20180810T093000
DTEND;TZID=Asia/Singapore:20180810T103000
DTSTAMP:20260418T032813
CREATED:20180807T040945Z
LAST-MODIFIED:20181005T073303Z
UID:23928-1533893400-1533897000@www.mbi.nus.edu.sg
SUMMARY:MBIw: Numerical modeling and simulations for motility of cell populations by Prof Tetsuya Hiraiwa
DESCRIPTION:MBI Weekly Meeting Seminar\nTime: 9.30am-10.30am\nDate: Friday\, 10 August 2018\nVenue: Level 5 Seminar Room\, T-Lab \nNumerical modeling and simulations for motility of cell populations\nby Prof Tetsuya Hiraiwa\, Assistant Professor\, The University of Tokyo\, Japan
URL:https://www.mbi.nus.edu.sg/event/numerical-modeling-and-simulations-for-motility-of-cell-populations-by-prof-tetsuya-hiraiwa/
LOCATION:MBI Seminar Room Lvl 5\, T-Lab\, Level 5\, 5A Engineering Drive 1\, Mechanobiology Institute\, National University of Singapore\, 117411\, Singapore
CATEGORIES:MBI Seminar,MBI Weekly Seminar
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BEGIN:VEVENT
DTSTART;TZID=Asia/Singapore:20180817T093000
DTEND;TZID=Asia/Singapore:20180817T103000
DTSTAMP:20260418T032813
CREATED:20180813T015624Z
LAST-MODIFIED:20181005T073508Z
UID:23954-1534498200-1534501800@www.mbi.nus.edu.sg
SUMMARY:MBIw: Signaling by WW domain-containing proteins in mechanobiology and human diseases by Prof Marius Sudol
DESCRIPTION:MBI Weekly Meeting Seminar\nTime: 9.30am-10.30am\nDate: Friday\, 17 August 2018\nVenue: Level 5 Seminar Room\, T-Lab \nSignaling by WW domain-containing proteins in mechanobiology and human diseases\nby Prof. Marius Sudol\, Co-Principal Investigator\, Mechanobiology Institute \n 
URL:https://www.mbi.nus.edu.sg/event/signaling-by-ww-domain-containing-proteins-in-mechanobiology-and-human-diseases-by-prof-marius-sudol/
LOCATION:MBI Seminar Room Lvl 5\, T-Lab\, Level 5\, 5A Engineering Drive 1\, Mechanobiology Institute\, National University of Singapore\, 117411\, Singapore
CATEGORIES:MBI Seminar,MBI Weekly Seminar
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Asia/Singapore:20180824T093000
DTEND;TZID=Asia/Singapore:20180824T103000
DTSTAMP:20260418T032813
CREATED:20180820T031119Z
LAST-MODIFIED:20181005T073550Z
UID:24050-1535103000-1535106600@www.mbi.nus.edu.sg
SUMMARY:MBIw: Elementary contractile unit and other challenging problems at the Physics Biology interface by Prof Jacques Prost
DESCRIPTION:MBI Weekly Meeting Seminar\nTime: 9.30am-10.30am\nDate: Friday\, 24 August 2018\nVenue: Level 5 Seminar Room\, T-Lab \nElementary contractile unit and other challenging problems at the Physics Biology interface\nby Prof. Jacques Prost\, Visiting Faculty\, Co-Principal Investigator\, Mechanobiology Institute\, Emeritus Professor\, Institut Curie
URL:https://www.mbi.nus.edu.sg/event/elementary-contractile-unit-and-other-challenging-problems-at-the-physics-biology-interface-by-prof-jacques-prost/
LOCATION:MBI Seminar Room Lvl 5\, T-Lab\, Level 5\, 5A Engineering Drive 1\, Mechanobiology Institute\, National University of Singapore\, 117411\, Singapore
CATEGORIES:MBI Weekly Seminar
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Asia/Singapore:20180831T093000
DTEND;TZID=Asia/Singapore:20180831T103000
DTSTAMP:20260418T032813
CREATED:20180827T034215Z
LAST-MODIFIED:20181005T073117Z
UID:24139-1535707800-1535711400@www.mbi.nus.edu.sg
SUMMARY:MBIw: EpCAM\, a key regulator of tissue biomechanics\, acts as a cortical organizer of cell contractility By Dr Delacour Delphine
DESCRIPTION:MBI Weekly Meeting Seminar\nTime: 9.30am-10.30am\nDate: Friday\, 31 August 2018\nVenue: Level 5 Seminar Room\, T-Lab \nEpCAM\, a key regulator of tissue biomechanics\, acts as a cortical organizer of cell contractility\nBy Dr. Delacour Delphine\, CNRS Researcher\, Institut Jacques Monod\, France \nIn monolayered epithelia\, differentiated cells are polarized and display a specific apico-basal organization.  To maintain cell polarization as well as cohesion of neighboring cells within the epithelial monolayer\, cells developed diverse adhesion complexes. However\, the epithelial monolayer is subjected to remodeling during organism development or tissue repair. In addition\, cell renewal\, cell rearrangements and cell extrusion occur to maintain the monolayer homeostasis. Consequently\, the epithelium has to constantly maintain its compartmentalization and to collectively adapt to its microenvironment to maintain its polarized and cohesive state. In recent years\, accumulating experimental evidences have led to recognition that mechanical properties of tissues have the power of directing a variety of cell functions including stem cell proliferation\, cell migration and differentiation. Various reports argue in favor of a participation of physical properties of the substrate\, such as substrate rigidity\, in the cell response for regulation of the epithelial monolayer integrity. Very little is known about the influence of the epithelial tissue geometry per se. \nOur aim is to study the influence of the tissue geometry on epithelial organization and to determine the regulatory mechanisms. These questions are addressed by developing integrated approaches at the cell biological\, biochemical and biophysical levels. As a tissue model\, we use the intestinal epithelium\, which constitutes a very good model to approach these different questions. It has a simple and regular finger-like architecture\, where proliferative and differentiate cells are distributed in distinct areas\, crypts and villi\, respectively. We mainly focus on the involvement of a protein candidate: EpCAM (Epithelial Cell Adhesion Molecule). Specifically expressed in monolayered epithelia in physiological conditions\, EpCAM was among the first discovered cancer markers in the 1970s\, and changes in its expression induce severe perturbation of epithelial tissue arrangement. Direct evidence of EpCAM involvement in epithelial morphogenesis came from a clinical study where mutations in EPCAM and subsequent loss of EpCAM expression have been correlated with the development of a rare infantile enteropathy\, the CTE (Congenital Tufting Enteropathy). The CTE intestinal epithelium displays unique morphological abnormalities\, materialized by formation of aberrant focal stacks of pseudo-multilayered epithelial cells\, named “tufts”\, making it an appealing pathological model that we use to understand the mechanisms of actions of EpCAM. \nUsing an intestinal cell line and 3D biomimetic substrates that recapitulate intestinal physical constraints\, we showed that “tuft”-like structures appear when EpCAM-deprived cells are specifically grown on 3D synthetic villi\, testifying of an enhanced mechanical stress provided by the particular topography of the monolayer substrate. EpCAM-silenced cells cultured on 3D synthetic villi can thus phenocopy CTE cellular and tissue defects. Moreover\, EpCAM loss-of-function abrogates polarized monolayer arrangement and a spatial perturbation of actomyosin occurs on villus-like 3D substrates. The alteration of epithelial contractile homeostasis is directly correlated to the development of tissue lesions\, since tissue-scale defects could be erased with contractility inhibitors. Data consequently tend to support a direct implication of EpCAM in the epithelial response to physical properties of the microenvironment. \nIn intestinal cell line and mouse and human intestinal biopsies\, we scrutinize the requirement of EpCAM for correct tissue organization and homeostasis. First\, we have showed that the absence of EpCAM provokes an unusual apico-basal polarity defects in mutant monolayers\, which stem from inappropriate actomyosin activity at tricellular junctions. Second\, we test EpCAM’s participation in early epithelial cell-substrate adhesion process and consequences on cell migration. The absence of EpCAM impairs proper single cell spreading on collagen-coated substrates with deleterious impact on front-rear polarity and migratory behaviour. In addition to a decreased protrusive activity\, the loss of EpCAM changes the morphometry of focal adhesions and abrogates proper stress fibre maturation. These modifications stem from a dysfunction of actomyosin regulation and a blocking of activated Rho zone at the cell cortex. In fact\, EpCAM acts upstream of the actomyosin apparatus and directly potentializes activated Rho recycling within the protrusion for efficient epithelial cell spreading. In parallel\, we investigate EpCAM’s participation in the homeostasis of the intestinal tissue. Within the proliferative compartment of mouse and human intestines\, EpCAM is enriched in bottom crypts\, more precisely at stem cell basolateral side\, suggesting its specific requirement for stem cell-substrate and cell-cell adhesions. Moreover\, the absence of EpCAM in CTE patients leads to clear disorganization of stem cell arrangement. Experiments pursued by using mouse EpCAM-KO 3D organoid primary cultures or CTE 3D organoid primary cultures demonstrate that EpCAM expression is required for correct de novo growth and maintenance of the intestinal stem cell niche. In-progress combination of organoids and optimized biomimetic 3D culture systems will allow more systematic analyses and live cell imaging of the intestinal niche and the differentiated epithelium along intestinal architecture. \nAltogether\, our work reveals that EpCAM acts as a key regulator of epithelial morphogenesis and homeostasis along tissue architecture by regulating actomyosin activity and actin cytoskeleton arrangement at the cell cortex.
URL:https://www.mbi.nus.edu.sg/event/epcam-a-key-regulator-of-tissue-biomechanics-acts-as-a-cortical-organizer-of-cell-contractility-by-dr-delacour-delphine/
LOCATION:MBI Seminar Room Lvl 5\, T-Lab\, Level 5\, 5A Engineering Drive 1\, Mechanobiology Institute\, National University of Singapore\, 117411\, Singapore
CATEGORIES:MBI Weekly Seminar
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