BDRC SEMINAR SEIRES
Sarah Escuin
Developmental Biology & Cancer Programme, ICH
4th December 2015, 1pm
June Lloyd Seminar Room (PUW4)
Exploring the role of the cytoskeleton during
mouse spinal neurulation
Abstract
The cytoskeleton is widely considered essential for neurulation and yet its role during mouse
spinal neural tube closure is unknown. We have shown that inhibiting Rho kinase signalling
or blocking F-actin disassembly resulted in spinal neural tube defects with accumulation of
apical actin filaments and abnormal adherens junctions in the neuroepithelium. Interestingly,
embryos mutant for Cofilin 1, an actin-binding protein that regulates assembly and
disassembly of actin filaments, also developed spinal neural tube defects, supporting a key
role for actin turnover during neural tube closure. Surprisingly, we have found that mouse
spinal neurulation does not require active actomyosin contraction and can proceed in the
absence of myosin contractile activity or with disrupted actin filaments. A precise regulation
of RhoA/ROCK/LIM kinase/cofilin signalling pathway is required for mouse spinal neurulation
to occur properly, with actin turnover and actomyosin disassembly within the
neuroepithelium playing an essential role.
Biosketch
After completing my master of sciences in developmental biology in Toulouse in 2002, I
moved to Strasbourg to do my Masters of Research in the team of Elisabeth GeorgesLabouesse at the Institute of Genetics and Molecular and Cellular Biology (IGBMC) where I
worked on integrin function and signalling in tissue morphogenesis. I stayed in the lab to do
my PhD and focused my work on the role of the Nck-interacting kinase, a partner of 1
integrin, in neuronal migration during mouse cerebral cortex development. In 2009 I joined
the group of Andy Copp and Nick Greene at the Institute of Child Health to analyse the role
of the cytoskeleton during neurulation.