UASt regulates expression of rl containing a serine instead of an arginine at position amino acid 80 as well as the "sevenmaker" gain-of-function mutation (D334N). The R68S mutation was initially identified in the yeast ERK, Mpk1, and renders Mpk1 intrinsically active; mutations at the equivalent residue of human ERK1 (R84) and ERK2 (R65) have been found in human tumors. The equivalent mutation to D334N is found in cancer patients (D321N in human ERK2).
Expressing rlR80S.D334N.UAS under the control of Scer\GAL4Bx-MS1096 causes dramatic wing vein hypertrophy, with formation of extra vein material, enhanced vein branching, and darker wing pigmentation.
rlR80S.D334N.UAS, Scer\GAL4Bx-MS1096 is a suppressor of visible | adult stage phenotype of RafDN.UAS, Scer\GAL4Bx-MS1096
rlR80S.D334N.UAS, Scer\GAL4Bx-MS1096 is a suppressor of abnormal size | adult stage phenotype of RafDN.UAS, Scer\GAL4Bx-MS1096
rlR80S.D334N.UAS, Scer\GAL4Bx-MS1096 is a suppressor of abnormal size | adult stage phenotype of Ras85DN17.UAS, Scer\GAL4Bx-MS1096
rlR80S.D334N.UAS, Scer\GAL4Bx-MS1096 is a suppressor | partially of abnormal size | adult stage phenotype of Dsor1GD9123, Scer\GAL4Bx-MS1096
rlR80S.D334N.UAS, Scer\GAL4Bx-MS1096 is a suppressor | partially of visible | adult stage phenotype of Dsor1GD9123, Scer\GAL4Bx-MS1096
rlR80S.D334N.UAS, Scer\GAL4Bx-MS1096 is a suppressor of visible | adult stage phenotype of Ras85DN17.UAS, Scer\GAL4Bx-MS1096
Dsor1GD9123, Scer\GAL4ey.PH, rlR80S.D334N.UAS has partially lethal - majority live phenotype
Scer\GAL4Act5C.PI, rlR80S.D334N.UAS, scrib1 has abnormal size | somatic clone | larval stage phenotype
Scer\GAL4Act5C.PI, rlR80S.D334N.UAS, scrib1 has neoplasia | somatic clone | adult stage phenotype
Dsor1GD9123, Scer\GAL4ey.PH, rlR80S.D334N.UAS has visible | adult stage phenotype
RafDN.UAS, Scer\GAL4Bx-MS1096, rlR80S.D334N.UAS has visible | adult stage phenotype
Ras85DN17.UAS, Scer\GAL4Bx-MS1096, rlR80S.D334N.UAS has visible | adult stage phenotype
rlR80S.D334N.UAS, Scer\GAL4Bx-MS1096 is a suppressor of wing phenotype of RafDN.UAS, Scer\GAL4Bx-MS1096
rlR80S.D334N.UAS, Scer\GAL4Bx-MS1096 is a suppressor of wing vein phenotype of RafDN.UAS, Scer\GAL4Bx-MS1096
rlR80S.D334N.UAS, Scer\GAL4Bx-MS1096 is a suppressor | partially of wing phenotype of Dsor1GD9123, Scer\GAL4Bx-MS1096
rlR80S.D334N.UAS, Scer\GAL4Bx-MS1096 is a suppressor of wing phenotype of Ras85DN17.UAS, Scer\GAL4Bx-MS1096
rlR80S.D334N.UAS, Scer\GAL4Bx-MS1096 is a suppressor of wing vein phenotype of Ras85DN17.UAS, Scer\GAL4Bx-MS1096
Dsor1GD9123, Scer\GAL4ey.PH, rlR80S.D334N.UAS has eye phenotype
Scer\GAL4Act5C.PI, rlR80S.D334N.UAS, scrib1 has adult abdomen phenotype
Scer\GAL4Act5C.PI, rlR80S.D334N.UAS, scrib1 has antennal disc phenotype
RafDN.UAS, Scer\GAL4Bx-MS1096, rlR80S.D334N.UAS has wing vein phenotype
Ras85DN17.UAS, Scer\GAL4Bx-MS1096, rlR80S.D334N.UAS has wing phenotype
Ras85DN17.UAS, Scer\GAL4Bx-MS1096, rlR80S.D334N.UAS has wing vein | ectopic phenotype
Ras85DN17.UAS, Scer\GAL4Bx-MS1096, rlR80S.D334N.UAS has wing vein phenotype
Scer\GAL4Act5C.PI, rlR80S.D334N.UAS, scrib1 has eye disc | somatic clone phenotype
The vestigial wing phenotype induced by the expression of Dsor1GD9123 under the control of Scer\GAL4Bx-MS1096 is considerably suppressed by the co-expression of rlR80S.D334N.UAS.
The pupal lethality of individuals expressing Dsor1GD9123 under the control of Scer\GAL4ey.PH is strongly rescued by the co-expression of rlR80S.D334N.UAS (majority live), although the adults show a (mostly mild) small eye phenotype.
The wing defects induced by the expression of Ras85DN17.UAS under the control of Scer\GAL4Bx-MS1096 (smaller wing and loss of L3-5 vein material are fully suppressed by the co-expression of rlR80S.D334N.UAS, even leading to extra vein material, with darker pigmentation).
scrib1 homozygous eye disc clones that also express rlR80S.D334N.UAS under the control of Scer\GAL4Act5C.PI are larger than clones only homozygous for scrib1. Double mutant antennal disc clones are readily detected, unlike scrib1 single mutant clones. Likewise, Individuals bearing double mutant clones show high abdominal accumulation of clonal cells, which is rare in the scrib1 single mutant clone condition.