The plakin domain of C. elegans VAB-10/plectin acts as a hub in a mechanotransduction pathway to promote morphogenesis

Plectin Mechanotransduction
DOI: 10.1242/dev.183780 Publication Date: 2019-11-29T15:35:13Z
ABSTRACT
Mechanical forces can elicit a mechanotransduction response through junction-associated proteins. In contrast to the wealth of knowledge available for focal adhesions and adherens junctions, much less is known about at hemidesmosomes. Here, we focus on C. elegans plectin homolog VAB-10A, only evolutionary conserved hemidesmosome component. elegans, muscle contractions induce pathway in epidermis We used CRISPR precisely remove spectrin repeats (SRs) or partially hidden Src homology 3 (SH3) domain within VAB-10 plakin domain. Deleting SH3 SR8 domains combination with mutations affecting mechanotransduction, just part SR5 shielding domain, induced embryonic elongation arrest because hemidesmosomes collapse. Notably, recruitment GIT-1, first player, requires transmembrane receptor LET-805. Furthermore, molecular dynamics simulations confirmed that acting could make central otherwise contact SR4, interaction. Collectively, our data strongly indicate plays role raise possibility VAB-10/plectin might act as mechanosensor.
SUPPLEMENTAL MATERIAL
Coming soon ....
REFERENCES (56)
CITATIONS (26)