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Fig. 7. Polarity of the BC cluster and proposed mechanism by which Fas2, Dlg and
Lgl control movement. (A-C') The polarity of the BC cluster is
demonstrated by the high levels of Amph in trailing BCs (tBCs) compared with
leading BCs (lBCs). Amph polarity is established just preceding BC
differentiation (stage 7-8; pBCs, presumptive BCs). (D) Model of a
delaminating BC cluster. At stage 7, Fas2 (orange), and Dlg and Lgl (blue) are
localized around the circumference of PCs and on lateral membranes of
presumptive BC epithelial cells. At stage 8, the BCs differentiate when Slbo
turns on. Fas2 is lost from BCs, and other anterior epithelial cells, except
PCs. Fas2 loss from BCs is crucial for Fas2 polarization to the leading half
of the PCs (morphogenetic switch, Fig.
2B). Dlg and Lgl become localized around the circumference of the
BCs. The PC Fas2-Dlg-Lgl complex acts through a putative BC receptor to
maintain cortical organization of Dlg and Lgl in BCs, which is crucial for
inhibiting rate of BC movement. Polarized communication between PCs and front
BCs assures timely delamination of the BC cluster. The polarized nature of the
cluster suggests that the work of the extension-retraction-contraction cycle
found in single cells may be distributed between multiple cells in the
migrating cluster and coordinated through Fas2 intercellular communication
(1). Another possibility is that polarized Fas2 signaling is required to
polarize front BCs in an active pattern similar to individual migrating cells,
with the back border cells playing a passive role (2).
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