During C. elegans embryogenesis, myoblasts initially form two rows along
the left and right lateral midlines and at ~290 min of development migrate
dorsally and ventrally to form the four muscle quadrants present upon hatching
(Sulston et al, 1983). As the myoblasts migrate they are still dividing, as are
many other cells in their immediate environment. This means the cell-cell contact
of cells during migration is dynamic and can vary from animal to animal
(Schnabel et al, 1997). This situation creates an environment where the
extracellular matrix (ECM) and cell surface contacts are in constant flux, which
begs the questions as to how these cells navigate unerringly to their final
destination.
In an attempt to identify genes mediating these migrations, I performed an
RNAi based screen targeting 776 genes predicted to be members of the
extracellular matrix (ECM), or one of its receptors. Using both feeding and
injection based RNAi, I was able to identify three genes of interest. Knockdowns
of F56B3.2 resulted in paralyzed animals with detached muscle, making it a good
candidate for a new component of the muscle attachment complex. F33G12.4
knockdowns resulted in an embryonic arrest phenotype with an abnormal muscle
lineage, possibly stemming from polarity defects. The only knockdown that
resulted in muscle migration defects was that for lam-2, which encodes for the
laminin gamma subunit. Analysis of the lam-2 knockdown, as well as
knockdowns for the other laminin subunits, revealed dorsal/ventral migration
defects as well as a posterior displacement of the anterior-most ventral muscle cells. Investigation of this posterior displacement has led to the identification of a
previously undescribed anterior muscle migration event and its dependency
upon the extension of muscle processes from the leading cells.
