Figure 8.

Ectopic Dimm expression blocks programmed cell death in a range of neurons as monitored in adult flies. (A) No corazonin immunoreactivity is detectable in the abdominal ganglia of control (Crz > w¹¹¹⁸) female flies, but there are 14–16 corazonin positive neurons present in the T3 segment of VNC after Dimm expression using a Crz-Gal4 driver. These neurons become larger after expressing combined Dimm/dInR. (B,C) EH expressing neurons also bypass apoptosis after Dimm expression (EH-Gal4 driver) and the size of their cell body increases after Dimm/dInR expression (controls not shown). The axons extending to the ring gland in larvae could be observed in adults terminating in the corpora cardiaca (CC) whereas the other set projected to the VNC. (D) Only one pair of leucokinin-producing SELKs is present in control adult flies (Lk > w¹¹¹⁸), whereas two or three pairs of SELKs are seen in the larval stage (not shown). After ectopic Dimm expression, three pairs of SELKs remain and become larger. Ectopic Dimm/dInR causes further increased cell body size. (E) The CCAP-immunoreactive neurons in the subesophageal ganglion normally undergo apoptosis within 3–5 days after adult emergence. Ectopic Dimm expression blocks this programmed cell death, and Dimm/dInR induces further cell growth of CCAP neurons. Scale bar = 20 μm.