BEGIN:VCALENDAR
VERSION:2.0
METHOD:PUBLISH
CALSCALE:GREGORIAN
PRODID:-//WordPress - MECv7.34.2//EN
X-ORIGINAL-URL:https://www.igf.cnrs.fr/
X-WR-CALNAME:IGF
X-WR-CALDESC:Institut de génomique fonctionnelle
X-WR-TIMEZONE:Europe/Paris
BEGIN:VTIMEZONE
TZID:Europe/Paris
X-LIC-LOCATION:Europe/Paris
BEGIN:DAYLIGHT
TZOFFSETFROM:+0100
TZOFFSETTO:+0200
TZNAME:CEST
DTSTART:20260329T030000
RRULE:FREQ=YEARLY;BYMONTH=03;BYDAY=-1SU
END:DAYLIGHT
BEGIN:STANDARD
TZOFFSETFROM:+0200
TZOFFSETTO:+0100
TZNAME:CET
DTSTART:20261025T020000
RRULE:FREQ=YEARLY;BYMONTH=10;BYDAY=4SU
END:STANDARD
END:VTIMEZONE
REFRESH-INTERVAL;VALUE=DURATION:PT1H
X-PUBLISHED-TTL:PT1H
X-MS-OLK-FORCEINSPECTOROPEN:TRUE
BEGIN:VEVENT
CLASS:PUBLIC
UID:MEC-040ca38cefb1d9226d79c05dd25469cb@igf.cnrs.fr
DTSTART;TZID=Europe/Paris:20260923T140000
DTEND;TZID=Europe/Paris:20260923T170000
DTSTAMP:20260818T132211Z
CREATED:20260818
LAST-MODIFIED:20260818
PRIORITY:5
SEQUENCE:5
TRANSP:OPAQUE
SUMMARY:Thesis – Victor BERNARD
DESCRIPTION:Role of hemodynamic forces and extracellular matrix in cardiac development and disease\nJury\n\nRomain CAPOULADE, Research scientist, Institut du Thorax, Nantes – Reviewer\nRobert KELLY, Research Director, IBDM, Marseille – Reviewer\nAnabela BENSIMON-BRITO, Research scientist, CBI, Toulouse – Examiner\nFlorence RUGGIERO, Research Director, IGFL, Lyon – Examiner\nPascal DE SANTA BARBARA, Research Director, PhyMedExp, University of Montpellier – Examiner\nAdèle FAUCHERRE, Research scientist, IGF, University of Montpellier – Thesis supervisor\n\nSummary\nHeart development relies on a close interplay between genetic programs and mechanical forces generated by blood flow. However, the mechanisms by which these forces regulate cardiac morphogenesis remain incompletely understood. During this thesis, we identified Crip2 as a novel cardiac mechanotransducer whose expression is regulated by hemodynamic forces through mechanosensitive ion channels. Loss of crip2 function in zebrafish and mice results in cardiovascular abnormalities, demonstrating its essential role in heart development. We also identified two rare CRIP2 variants in patients with congenital heart defects and developed an in vivo model to assess their pathogenicity. Investigation of the pathways regulated by Crip2 revealed a link with elastin (ELN), a major component of the cardiovascular extracellular matrix. Using an elna/b knockout zebrafish model, we demonstrated the pathogenicity of two human ELN variants, one of which is associated with bicuspid aortic valve, providing the first evidence of a direct link between ELN and this malformation. Together, these findings identify a novel molecular axis linking hemodynamic forces, mechanotransduction, and the extracellular matrix, while establishing new functional models for the interpretation of genetic variants involved in congenital heart defects.\n
URL:https://www.igf.cnrs.fr/en/events/thesis-victor-bernard/
CATEGORIES:Thesis
ATTACH;FMTTYPE=image/jpeg:https://www.igf.cnrs.fr/wp-content/uploads/2026/08/photo-Victor-Bernard-e1787051986328.jpg
END:VEVENT
END:VCALENDAR