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VERSION:2.0
PRODID:Icfo
X-PUBLISHED-TTL:P1W
BEGIN:VEVENT
UID:69d4b0e4bd40f
DTSTART:20240312T140000Z
SEQUENCE:0
TRANSP:OPAQUE
LOCATION:ICFO Auditorium
SUMMARY:ICFO | NEUS SANFELIU CERDÁN
CLASS:PUBLIC
DESCRIPTION:In recent years\, our understanding of the ion channels and rec
 eptors that orchestrate the conversion of physical stimuli into physiologi
 cal signals has deepened significantly. Nevertheless\, there remains some 
 ambiguity regarding the precise mechanism by which mechanical stresses rea
 ch the molecular mechanosensors. While it is well-established that many me
 chanosensitive ion channels respond to increased plasma membrane tension\,
  emerging evidence underscores the crucial role played by the cytoskeleton
  within sensory cells. In this thesis\, we asked how animals perceive mech
 anical stress\, with specific focus on touch sensation. Our primary object
 ive was to unravel the molecular and the mechanical pathways responsible f
 or transmitting force within the touch receptor neurons of the nematode Ca
 enorhabditis elegans. For over a decade\, it has been postulated that the 
 pore-forming subunit of the mechanoelectrical transduction channel forms a
  connection with the cytoskeleton through a highly conserved and widesprea
 d protein known as MEC-2\, which bears structural similarities to Stomatin
 . Our study presents compelling evidence that MEC-2 assembles in liquid co
 ndensates that experience a shift in rigidity\, transitioning from a fluid
 -like pool that allows transport along neurons to solid-like states that a
 re mechanoelectrically active. We provide a new physiologically relevant c
 ontext in which biomolecular condensates tune their function upon maturati
 on and facilitate neuronal mechanotransduction in response to tactile stim
 uli. In order to contextualize the function of MEC-2 in force transmission
 \, we developed a genetically encoded tension sensor module\, which reveal
 ed that only stiffened condensates\, as opposed to fluid-like ones\, are c
 apable of transmitting force within living organisms. Notably\, this stiff
 ening process does not occur autonomously. Within this study\, we showed t
 hat this transition is instigated by a specific SH3 motif of UNC-89\, a pr
 otein homologous to Titin and Obscurin\, through a direct interaction with
  a proline-rich domain located in the C-terminal region of MEC-2. We propo
 se that this change in rigidity serves a vital physiological function by c
 ontributing to the transmission of forces that vary in frequency during to
 uch to the animal's body wall. Together\, our data introduces a novel pers
 pective on the significance of the MEC-2 liquid-to-solid phase transition 
 in the realm of mechanotransduction. It also presents a new conceptual fra
 mework for understanding how animals\, in a broader sense\, perceive and r
 espond to mechanical stresses.\n&nbsp\;\nTuesday March 12\, 15:00 h. ICFO 
 Auditorium and Online (Teams)\nThesis Director: Prof Dr. Michael Krieg
DTSTAMP:20260407T072316Z
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