Figure 4.

Invasion is not driven by haemocyte recruitment and TNF/Eiger-dependent signalling. (a) Possible model of extrinsic signalling from haemocytes to JNK activation in tumours. In the absence of Ras^V12, activated JNK leads to cell death, whereas in its presence, cell death is suppressed and JNK promotes Mmp1 expression. Consequently, JNK and Ras^V12 cooperate to drive tumour cell invasion. TNF/Eiger-secreting haemocytes that are recruited to sites of certain primary tumours, for example scrib^−/− Ras^V12, have been reported to be capable of providing extrinsic cues that trigger JNK activation, raising the possibility this is also the case for pico Ras^V12 tumours. (b) Images of dissected brains showing distribution of haemocytes, as detected with an anti-NimC1 P1 antibody. Haemocytes were not detected in brains expressing pico or Ras^V12 alone. In pico or Ras^V12 brains, haemocytes were sometimes observed at sites of invasion, but this was not a necessary outcome. (c) Graph summarizing extent of invasion in the different genotypes (n=100 brains of each type).