72
M. Affolter
requires that groups of cells are instructed with respect to distinct routes,
which they have to follow. The highly stereotyped development of the
tracheal system combined with the powerful genetic model of Drosophila should allow a molecular dissection of this process and lead to a
better understanding of how cells recognize and interpret migration
cues. One of our main interests is to find out whether migration during
tracheal development is controlled in an axis-specific fashion, as has
been observed for a number of cells in C. elegans (see above).
Mutations in a number of genes have been reported to cause abnormal development of the tracheal system. The breathless (btl) gene is
expressed in all tracheal cells and encodes a Drosophila fibroblast
growth factor receptor (DFGF-R; Klambt et al. 1992). In the absence of
btl function, tracheal cell division as well as general tracheal cell fate is
unaffected, but the cells fail to migrate and consequently no branches
are formed. Initial studies with activated components of the FGF signaling pathway suggested that the normal activity of btl in promoting cell
migration does not require spatially restricted cues (Reichmann-Fried et
al. 1994). However, more recent results indicate that BTL is activated by
a spatially restricted FGF-like ligand, the product of the branchless (bnl)
gene (Sutherland et al. 1996). The dynamic expression of bnl at each
position where a new branch will form and grow out, combined with the
results obtained from ectopic expression experiments, suggest that BNL
acts as a chemoattractive guidance molecule (Sutherland et al. 1996).
5.2.2 Isolation of Genes
Required for Directed Tracheal Cell Migration
To isolate components required for directed cell migration, we have
analyzed, over the last five years, a large number of mutations for
possible tracheal defects using as a tool an antibody that outlines the
developing trachea. In these various screens, we have isolated mutations
giving rise to two qualitatively different tracheal phenotypes: (a) tracheal cell migration completely absent, and (b) tracheal cell migration
defective in distinct directions only. The characterization of these mutations and the isolation of the corresponding wild-type gene products will
be discussed separately.
M. Affolter
requires that groups of cells are instructed with respect to distinct routes,
which they have to follow. The highly stereotyped development of the
tracheal system combined with the powerful genetic model of Drosophila should allow a molecular dissection of this process and lead to a
better understanding of how cells recognize and interpret migration
cues. One of our main interests is to find out whether migration during
tracheal development is controlled in an axis-specific fashion, as has
been observed for a number of cells in C. elegans (see above).
Mutations in a number of genes have been reported to cause abnormal development of the tracheal system. The breathless (btl) gene is
expressed in all tracheal cells and encodes a Drosophila fibroblast
growth factor receptor (DFGF-R; Klambt et al. 1992). In the absence of
btl function, tracheal cell division as well as general tracheal cell fate is
unaffected, but the cells fail to migrate and consequently no branches
are formed. Initial studies with activated components of the FGF signaling pathway suggested that the normal activity of btl in promoting cell
migration does not require spatially restricted cues (Reichmann-Fried et
al. 1994). However, more recent results indicate that BTL is activated by
a spatially restricted FGF-like ligand, the product of the branchless (bnl)
gene (Sutherland et al. 1996). The dynamic expression of bnl at each
position where a new branch will form and grow out, combined with the
results obtained from ectopic expression experiments, suggest that BNL
acts as a chemoattractive guidance molecule (Sutherland et al. 1996).
5.2.2 Isolation of Genes
Required for Directed Tracheal Cell Migration
To isolate components required for directed cell migration, we have
analyzed, over the last five years, a large number of mutations for
possible tracheal defects using as a tool an antibody that outlines the
developing trachea. In these various screens, we have isolated mutations
giving rise to two qualitatively different tracheal phenotypes: (a) tracheal cell migration completely absent, and (b) tracheal cell migration
defective in distinct directions only. The characterization of these mutations and the isolation of the corresponding wild-type gene products will
be discussed separately.