Worm Breeder's Gazette 11(5): 70

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

Electron Microscopy of Basal Laminae in epi-1 Mutants

David Hall and Edward Hedgecock

Basal laminae first appear at gastrulation, separating the tissue 
layers (endoderm, mesoderm, ectoderm) and regulating their 
morphogenesis.  In particular, a delimiting basal lamina is a 
prerequisite for tissue polarization, i.e., conversion from mesenchyme 
to epithelium (1).  Embryonic hypodermis, pharynx, and intestine 
polarize during gastrulation, but gonads polarize late in larval 
development.  As a consequence, gonadal myoepithelia are large and 
accessible throughout their morphogenesis.  
Several known mutants are defective in epithelialization of male or 
female gonads (2).  In epi-1(rh152), polarization is defective and 
most adults are sterile.  The basal lamina surrounding the germ cells 
is weak and sometimes herniates, allowing germ cells to escape into 
the coelomic cavity.  In a stronger allele, rh165, the basal lamina of 
the gonad is breached entirely and germ cells proliferate throughout 
the body cavity, typically in close apposition to other tissues.  
Interestingly, only a minority of germ cells enter meiosis.  
We have examined L4 larvae and adults from rh165 strains by electron 
microscopy.  Although pharyngeal basal laminae appear relatively 
intact, other basal laminae are breached at numerous sites.  The body 
cavity contains sheets of detached matrix arranged in large onion-like 
stacks or whorls.  Whereas wildtype tissues are separated by apposed 
basal laminae, mutant tissues, e.g., hypodermis and intestine, often 
fuse together at places of direct cell contact.  Without an intact 
hypodermal basal lamina, axon fascicles are frequently displaced into 
the body interior.  Myofilaments, anchored at muscle-hypodermal 
appositions in wild type, assemble ectopically at muscle-intestinal 
appositions in these mutants.  
Because gonadogenesis is severely disturbed, rh165 homozygotes are 
sterile.  It is unknown whether maternal expression of epi-1(+) is 
necessary for the formation of embryonic epithelia.  
epi-1 is very closely linked to mec-3 on LGIV.  John Yochem and Iva 
Greenwald (Princeton University) have identified a laminin A chain 
gene approximately 200 kb rightward of mec-3 (3).  Based on the 
cellular phenotype, and coincidence of genetic and physical map 
positions, we suspect epi-1 alleles may be mutations of this laminin A 
gene.  Although specific functions of individual laminin chains are 
largely unknown, A chains are proposed to organize epithelial 
polarization (4).