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Summary: creased proliferation, growth, and survival by
means other than RasV12
are not sufficient to
cause the metastatic progression of scrib/
cells.
Thus, the metastasis-promoting effect of scrib
inactivation is highly dependent on its specific
cooperation with the RasV12
allele. Moreover,
aside from its known effects on proliferation,
growth, and survival, RasV12
may function
through an as yet undefined cellular mechanism
to elicit metastatic progression in scrib/
cells.
It has proven difficult to systematically
study the genetic basis of metastasis with the
currently available techniques. The Drosophila
system described here circumvents the compli-
cation of acquired background mutations,
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