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Correspondence to: Graham H. Thomas, Departments of Biology and of Biochemistry and Molecular Biology, The Pennsylvania State University, 208 Erwin W. Mueller Laboratory, University Park, PA 16802. Tel:(814) 863-0716 Fax:(814) 865-9131 E-mail:gxt5{at}psu.edu.
Changes in cell shape and position drive morphogenesis in epithelia and depend on the polarized nature of its constituent cells. The spectrin-based membrane skeleton is thought to be a key player in the establishment and/or maintenance of cell shape and polarity. We report that apical ßHeavy-spectrin (ßH), a terminal web protein that is also associated with the zonula adherens, is essential for normal epithelial morphogenesis of the Drosophila follicle cell epithelium during oogenesis. Elimination of ßH by the karst mutation prevents apical constriction of the follicle cells during mid-oogenesis, and is accompanied by a gross breakup of the zonula adherens. We also report that the integrity of the migratory border cell cluster, a group of anterior follicle cells that delaminates from the follicle epithelium, is disrupted.
Elimination of ßH prevents the stable recruitment of 
-spectrin to the apical domain, but does not result in a loss of apicobasal polarity, as would be predicted from current models describing the role of spectrin in the establishment of cell polarity. These results demonstrate a direct role for apical (ßH)2-spectrin in epithelial morphogenesis driven by apical contraction, and suggest that apical and basolateral spectrin do not play identical roles in the generation of apicobasal polarity.
Key Words: spectrin, oogenesis, cell polarity, zonula adherens, morphogenesis
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