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Fig. 8. Functional replacement of Neur by D-mib. Shown are dorsal thoraces from
adult flies (A-D) or 36-hour APF pupae (E-P) containing
ubx-FLP-generated MARCM clones of cells that are simultaneously
mutant for neur and express sca-Gal4 and relevant
UAS-transgenes (please refer to the Materials and methods for details of the
genetics). (A) Clones of the weak allele neurA101 exhibit
a bristle tufting phenotype (asterisk), wherein multiple sensory organs are
present at individual positions. (B) The tufting phenotype of
neurA101 clones is completely rescued by expression of
UAS-neur. (C) Clones of the stronger allele
neurIF65 are bald (asterisk), due to conversion of outer
sensory cell fates into neurons. (D) The balding phenotype of
neurIF65 clones is rescued back to a mild-tufting
phenotype (asterisk) by expression of UAS-D-mib. (E-G)
neurIF65 sensory clusters marked by GFP expression (due to
MARCM activation of sca-Gal4>UAS-pon-GFP: E, asterisk) fail to
express Su(H), a marker of socket cell fate (red, F,G); arrow in F indicates a
Su(H)+ nucleus. (H-J) neurIF65 sensory clusters
with sensory specific expression of D-mib show rescue of Su(H) expression.
Note that small clusters of Su(H)+ cells are usually seen,
indicating a partial rescue of the strong neurIF65 lateral
inhibition defect. (K-P) X-Z confocal sections through individual
neur mutant sensory clusters expressing GFP and stained for ELAV, a
neuronal marker. (K,N) A single neuron and the two large cell bodies of the
socket and shaft cells are present in wild type. (L,O) A large mass of neurons
is found in a neurIF65 sensory cluster, and large cell
bodies indicative of outer cell fates are absent. (M,P) Rescue of the
neurIF65 neurogenic defect and socket/shaft
differentiation by ectopic D-mib.