Worm Breeder's Gazette 11(3): 67

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Cell Autonomous Defects in Muscle Differentiation

Edward Hedgecock

Figure 1

Zygotic lethal, emb(rh54: III), mutants arrest during embryonic 
elongation.  Embryos can pump and hatch but are paralyzed and soon die.
Mosaics were generated using the unstable free duplication, sDp3, 
covering dpy-1 emb(rh54) ncl-1 chromosomes (duplication losses in 
individual mosaics are shown by stars below).  AB(-), EMS(-), and C(-) 
larvae are viable and reach adulthood.  (D(-) larvae have not yet been 
observed but are also expected to be viable.)  Cell autonomous defects 
were observed in the excretory cell, gonad, and non-pharyngeal muscles.
Mutant excretory cells fail to extend canals along the hypodermis 
but instead form a convoluted canal within their cell body.  Mutant 
gonads have apparently normal cell lineages, but uterus, spermatheca, 
and ovarian sheath fail to assemble and flatten normally.  Mutant body 
muscles attach to the hypodermis but fail to spread and form a 
myofilament lattice.  Similarly, mutant anal depressor muscles attach 
normally but have little if any birefringence using polarized light.  
Mutant sex myoblasts (SMs) fail to migrate to the hermaphrodite gonad 
but generate apparently normal lineages in situ.  Vulval and uterine 
muscles remain attached to the body wall but are apparently not 
contractile.
These defects suggest that emb(rh54) is required for the 
differentiation of certain cells, including the expression or assembly 
of myofilaments in non-pharyngeal muscles, SM migrations, and 
excretory canal outgrowth.  It is somewhat surprising that these 
different phenotypes should occur together.  Zygotic mutants on LGIII 
with similar embryonic phenotypes, reported independently by J.  
Rothman and by B.  Williams and R.  Waterston (pat-2), could be 
allelic to emb (rh54).[See Figure 1]

Figure 1