A. Rodriguez et al., IDENTIFICATION OF IMMUNE-SYSTEM AND RESPONSE GENES, AND NOVEL MUTATIONS CAUSING MELANOTIC TUMOR-FORMATION IN DROSOPHILA-MELANOGASTER, Genetics, 143(2), 1996, pp. 929-940
We are using Drosophila as a model system for analysis of immunity and
tumor formation and have conducted two types of screens using enhance
r detector strains to find genes related to these processes: genes exp
ressed in the immune system (type A; hemocytes, lymph glands and fat b
ody) and genes increased in expression by bacterial infection (type B)
. For type A, tissue-specific reporter gene activity was determined. F
or type B, a variation of enhancer detection was devised in which beta
-galactosidase is assayed spectrophotometrically with and without bact
erial infection. Because of immune system involvement in melanotic tum
or formation, a third type was hypothesized to be found among types A
and B: genes that, when mutated, have a melanotic tumor phenotype. Enh
ancer detector strains (2800) were screened for type A, 900 for B, and
11 retained for further analysis. Complementation tests, cytological
mapping, P-element mobilization, and determination of lethal phase and
mutant phenotype have identified six novel genes, Dorothy, wizard, to
te, viking; Thor and dappled, and one previously identified gene, Coll
agen IV. All are associated with reporter gene expression in at least
one immune system tissue. Thor has increased expression upon infection
. Mutations of wizard and dapped have a melanotic tumor phenotype.