Formation of the inner ear from the otic placode differs from invagina
tion of other cup-shaped organ primordia. Activation of the actin cyto
skeleton seems to play a limited role because precocious invagination
does not occur upon treatment with activators of a contractile event a
nd cannot be prevented by inhibitors. In this study, the possibility t
hat invagination is mediated by changes in the surrounding mesenchyme
was tested by treating embryos with agents which interfere with the in
tegrity of extracellular matrix. Enzymes degrading hyaluronate and/or
chondroitin sulfate were microinjected into the otic region prior to f
olding. Synthesis of chondroitin sulfate proteoglycan was inhibited by
microinjection of beta-xyloside, All treatments inhibited otic pit fo
rmation by interfering with fold formation within the placode, Immunoc
ytochemical procedures showed depletion of the appropriate extracellul
ar matrix components for a short time period after enzyme treatments a
nd for up to 24 hr after beta-xyloside injection. Invagination of the
otic primordium is concluded to be controlled in part by anchorage of
the epithelium to adjacent structures and possibly by expansion of the
mesenchymal extracellular matrix. (C) 1995 Wiley-Liss, Inc.