Fig. 7. The inappropriate defasciculation observed in mutants with reduced MMP
activity is suppressed by increasing interaxonal adhesion. In each
micrograph, two abdominal hemisegments of stage 17 dissected embryos stained
with
-FasII to label the motor projections are shown with anterior left
and dorsal up. Below each image are schematics of the observed phenotypes with
motor axons in brown and muscles represented by gray boxes.
(A,D) Wild-type embryo exhibiting normal ISNb morphology.
(B,E) elav>Fas2 mutant embryos have increased motor
axon adhesion. (C,F) elav>Fas2, Timp embryos exhibit
phenotypes consistent with weakened interaxonal adhesion relative to
elav>Fas2 embryos. (G,J)
Mmp2W307*/Mmp2Df mutant embryos have
loosely bundled ISNb axons and ectopic branching. (H,K) The ISNb
of Sema-1aP1/Sema-1aP1 mutant embryos
exhibits hyperfasciculation and does not properly innervate its muscle
targets. (I,L) In Sema-1aP1
Mmp2W307*/+ Mmp2Df mutant embryos, ISNb morphology
resembles that of wild-type embryos. Note that these embryos have more tightly
bundled nerves than do the Mmp2 homozygous mutants shown in G. Scale
bar: 15 µm.