TABLE 5.
Genetic interactions between GMR-dRetMEN2B P-element modifiers and GMR-dRetWT, GMR-dRetMEN2A, and dEGFRElp
| Gene/allele | GMR-dRetMEN2B | GMR-dRetMEN2A | GMR-dRetWT | MEN2B specific | dEGFRElp |
|---|---|---|---|---|---|
| msnj1E2 | ME(88) | WE(18) | WE(50) | No | WE |
| dCskj1D8 | WE(76) | N | WE(52) | No | N |
| hhrJ413 | WE(84) | WE(92) | ME(100) | No | SE |
| crbj1B5 | WE(93) | WE(69) | WE(100) | No | N |
| l(3)j2D5 | ME(95) | WE(76) | WE(82) | No | WS |
| drkk02401 | SS(95) | N | N? | Noa | WS |
| spis3547 | WS(86) | WS(65) | No | MEb | |
| pxk08316 | WS(73) | N | WS(54) | No | WE |
| Sk09538 | WS(67) | WS(14) | N | Noa | MEb |
| kismetk10237 | WS(80) | WS(71) | N | No | ND |
| drkk13809 | WS(100) | N | WS(23) | No | N |
| ebik16213 | SS(85) | WS(65) | WS(18) | No | N |
| Ras85D06677 | WS(76) | MS(100) | No | ND | |
| l(3)06803 | WS(95) | MS(91) | No | WE | |
| l(3)06906 | WS(100) | MS(100) | No | N | |
| l(3)j5B6 | WE(97) | ME(100) | No | N | |
| l(3)j4B9 | WE(95) | WE(68) | No | N | |
| neurj6B12 | WE(94) | WE(47) | No | N | |
| Pp1-87Bj6E7 | WE(85) | WE(29) | No | WE | |
| scribj7B3 | WE(98) | WE(45) | No | ME | |
| Sin3A08269 | WE(86) | WE(100) | WE(77) | No | N |
| drk10626 | SS(100) | WS(24) | MS(100) | No | N |
| l(3)S005504 | ME(91) | WE(30) | WE(70) | No | N |
| l(3)S001405 | WE(95) | N | WE(58) | No | WE |
| l(3)S003704 | WE(94) | N | ND | WE | |
| l(3)S000718 | WE(96) | N | WE(47) | No | N |
| l(3)S009515 | WE(93) | N | WE(62) | No | N |
| l(3)S000710 | WE(82) | WE(26) | No | N | |
| l(3)S012805 | WE(100) | N | WE(97) | No | N |
| l(3)S016805 | WE(88) | WE(12) | WE(96) | No | N |
| l(3)S023708 | ME(94) | WE(15) | N | No | N |
| l(3)S023549 | WE(82) | WE(50) | No | N | |
| l(3)S024833 | WE(96) | WE(33) | No | N | |
| l(3)S023901 | WE(100) | WS(39) | WE(79) | No | N |
| l(3)S022231 | WE(91) | N | WE(80) | No | N |
| l(3)S024503 | WE(92) | N | ND | N | |
| l(3)S026238 | WE(100) | N | WE(65) | No | N |
| l(3)S026421 | WE(94) | N | WE(90) | No | N |
| l(3)S024329 | WE(88) | WE(71) | WE(52) | No | N |
| l(3)S049706 | ME(85) | N | WE(82) | No | ND |
| l(3)S054513 | WE(79) | N | ND | N | |
| l(3)S046604 | WE(96) | WE(52) | ME(95) | No | N |
| l(3)S049902 | WE(93) | N | WE(35) | No | WE |
| DlS049520 | WS(85) | WS(100) | No | N | |
| bonS048706 | WE(93) | WE(50) | WE(81) | No | WS |
| l(3)S047526 | ME(100) | N | SE(100) | No | WE |
| l(3)S066607 | WE(96) | WE(22) | WE(96) | No | N |
| l(3)S057101 | WE(95) | N | WE(59) | No | WE |
| l(3)S068808 | WE(93) | WE(32) | WE(84) | No | N |
| l(3)S083407 | WE(90) | WE(24) | No | N | |
| l(3)S063512 | WE(81) | WE(15) | WE(75) | No | ME |
| l(3)S056113 | WE(88) | N | WE(50) | No | N |
| l(3)S090101 | WE(100) | WE(38) | WE(81) | No | N |
| l(3)S090114 | WE(79) | N | WE(76) | No | N |
| l(3)S141715 | WE(84) | N | ND | N | |
| l(3)S136603 | WE(97) | N | WE(90) | No | N |
| l(3)S092708 | WE(94) | N | WE(83) | No | N |
| l(3)S003003 | WE(82) | N | WE(100) | No | WE |
| l(3)S050116 | WE(97) | WE(49) | WE(46) | No | N |
| l(3)S142909 | WE(84) | N | WE(85) | No | N |
| l(3)S147412 | WE(91) | WE(39) | WE(85) | No | N |
| l(3)S145911 | WE(91) | N | WE(69) | No | N |
| l(3)S146006 | WS(100) | MS(100) | WS(52) | No | N |
| l(3)S135703 | WE(86) | N | WE(81) | No | N |
| l(3)S133117 | WE(85) | WE(45) | WE(81) | No | N |
| l(3)S130910 | WE(85) | WS(30) | WE(40) | No | WE |
Each GMR-dRetMEN2B modifier was crossed to GMR-dRetWT and/or GMR-dRetMEN2A constructs to determine the specificity of dRetMEN2 genetic interactions. Not all P-element lines could be tested since some lines died and were no longer available from the stock centers: these are indicated as ND (not determined).
Other alleles of Star and drk interact with GMR-RetMEN2A (Table 6). This is probably due to the hypomorphic nature of the alleles isolated in the screen.
Some positive regulators of the Ras pathway such as spitz actually dominantly enhanced dEGFRElp, demonstrating that dEGFRElp does not show simple linear interactions with Ras-ERK kinase pathway components. This suggests that dEGFRElp does not constitute a simple gain-of-function model for RTK signaling; this may reflect negative feedback loops that regulate dEGFR signaling (Spencer and Cagan 2003).