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. 2023 May 24;51(3):983–993. doi: 10.1042/BST20220719

Figure 3. Two Hh transport models to explain the Hhs inability to cross a field of HSPG-deficient cells (labelled black) in the wing disc.

Figure 3.

(A) The cytoneme model posits that Ihog (yellow) expressed on Hh-transporting basolateral cytonemes interact with HSPGs (Hh is shown as blue dots). This interaction is required to stabilize cytonemes. Thereby, lack of HSPGs prevents cytonemes to cross the HSPG-deficient field of cells. Small clones of HSPG mutant cells are crossed, however, and signalling anterior to the clone can be observed (bottom left, [27]). The ability of cytonemes to cross small clones of HSPG-deficient cells, in contrast with endogenously expressed Hh that does not [20], may be explained by Ihog overexpression required for cytoneme visualization in this experimental setup [27,32]. (B) The ‘Hh relay' model suggests strongly impaired apical Hh hand-over to clonal cells that do not express acceptor HSPGs or express undersulphated HSPGs. As a consequence, Hh accumulates at the clone border and fails to signal to normal tissue anterior to the clone.