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Abstract
Activation of cAMP-dependent protein kinase (PKA) by cell-permeable analogs of cAMP
causes early and mid-vitellogenic follicles of Hyalophora cecropia to terminate vitellogenin
uptake [[Wang and Telfer, 1996], Insect Biochem. Mol. Biol. 26, 85-94 (1996)]. The
response is shown here to entail the formation of an epithelial diffusion barrier.
Follicle cells that have been loosely organized to provide intercellular pathways
for the movement of vitellogenin to the oocyte surface transform into a tight epithelium
within 1-2h of exposure to PKA activators. The follicle cells can now prevent the
escape of Lucifer yellow CH that has been iontophoresed into the space surrounding
the oocyte, and the entry of labeled vitellogenin from the medium. As they form this
functional equivalent of a tight junction, the follicle cells further reduce the intercellular
spaces by enlarging and pressing against each other, and by slowing the secretion
of the sulfated glycosaminoglycan matrix that separates them during vitellogenesis.
The activation of PKA in early and mid-vitellogenic follicles thus appears to trigger
prematurely a set of changes that do not normally occur until the follicle has grown
to a length of about 2.0mm.