Table A2.
The simulated effect of different mutations.
| Case | 1 | 2 | VPC | F | Muv | Vul | Egl | Wild type | Mutants |
|---|---|---|---|---|---|---|---|---|---|
| 1 | 0 | 0 | 0 | 0 | 0 | 1 | 1 | 0 | Mutants in this category imply that the Pn.p cells did not form |
| 2 | 0 | 0 | 0 | 1 | 0 | 1 | 1 | 0 | Mutations that cause EFF-1 to be constitutively active: eff1(1), CSL(0);ref-2(0);elt-6(0); egl-18(0) |
| 3 | 0 | 0 | 1 | 0 | 0 | 1 | 1 | 0 | |
| 4 | 0 | 0 | 1 | 1 | 0 | 1 | 1 | 0 | |
| 5 | 0 | 1 | 0 | 0 | 1 | 0 | 1 | 0 | Ras mutations upstream of RGL-1 which cause RGL-1 to be activated:let23(1), let-60(1), lin-3*(1), sem-5(1), sos-1(1) |
| 6 | 0 | 1 | 0 | 1 | 0 | 1 | 1 | 0 | No Ras signaling and no WNT signaling or complete loss of lin-39 activity: lin-3(0);cwn-1*(0);cwn-2*(0);egl-20*(0);lin-44*(0);mom-2*(0), lin-39(0) |
| 7 | 0 | 1 | 1 | 0 | 0 | 1 | 1 | 0 | Mutations that do not allow lin-39 to be completly activated: ceh-13(1), ceh-20(0), egl-20*(2), let-23(0), let-23ml(0), let-60(0), lin-1(0), lin-10(0), lin-2(0), lin-25(0), lin-3(0), lin-31(0), lin-39(1), lin-39a(0), lin-39a(1), lin-45(0), lin-45(1), lin-7(0), mab-5(1), mc(0), mek-2(0), mek-2(1), mpk-1(0), mpk-1(1), pjw5(0), pjw5(1), sem-5(0), sos-1(0), sur-2(0), unc-62(0) |
| 8 | 0 | 1 | 1 | 1 | 0 | 1 | 1 | 0 | Loss of Wnt signaling: apr-1(1), cwn-1*(0);cwn-2*(0);egl-20*(0);lin-44*(0);mom-2*(0), gsk-3(1), lit-1(0), mig-5(0), pop-1(0), pop-1b(0), wrm-1(0) |
| 9 | 1 | 0 | 0 | 0 | 1 | 0 | 1 | 0 | Mutations in Ras signaling genes that cause phosphorilated lin-39 to remain highly active: let-23(3), let-60(3), lin-3*(3), lin-39a(2), lin-45(3), mek-2(3), mpk-1(2), sem-5(3), sos-1(3) |
| 10 | 1 | 0 | 0 | 1 | 1 | 1 | 1 | 0 | |
| 11 | 1 | 0 | 1 | 0 | 1 | 0 | 1 | 0 | Loss of NOTCH signaling or loss of Ras regulation in second fate cells: csl(0), lin-11(0), lip-1(0) |
| 12 | 1 | 0 | 1 | 1 | 1 | 1 | 1 | 0 | |
| 13 | 1 | 1 | 0 | 0 | 1 | 0 | 1 | 0 | DSL ligands present in the environment, or mutations that cause Ras signaling to be too active to guarantee the determination of the second fate but not high enough to cause all cells to acquire the first fate: apx-1*(0);dsl-1*(0);lag-2*(0);lin-3*(2), apx-1*(1), dsl-1*(1), lag-2*(1), csl(1), let-23(2), let-60(2), lin-12_2(1), lin-12_3(1), lin-3(2), lin-45(2), mek-2(2), ral-1(1), rgl-1(1), sem-5(2), sos-1(2) |
| 14 | 1 | 1 | 0 | 1 | 0 | 1 | 0 | 0 | Loss of ref-2 fusion control: ref-2(0) |
| 15 | 1 | 1 | 1 | 0 | 0 | 0 | 0 | 1 | apx-1*(0), cwn-1*(0), cwn-2*(0), dsl-1*(0), lag-2*(0), lin-44*(0), mom-2*(0), aph-1(0), aph-2(0), aph-2(1), apr-1(0), apx-1(0), apx-1(1), ark-1(0), ark-1(1), bar-1(0), bar-1(0);sys-1(1), bar-1(1), cam-1(0), cam-1(1), dpy-23(0), dpy-23(0);gap-1(0), dsl-1(0), dsl-1(1), eff-1(0), egl-17(0), egl-17(1), egl-18(0), egl-18(0);elt-6(0), egl-18(1), egl-20*(0), elt-6(0), elt-6(1), gap-1(0), gsk-3(0), kin-19(0), kin-19(1), ksr-1(0), ksr-1(0);ksr-2(0), ksr-2(0), lag-1(0), lag-2(0), lag-2(1), lin-11(1), lin-12(0), lin-12(1), lin-12_1(0), lin-12_1(1), lin-12_2(0), lin12-_3(0), lin-14(0), lin-14(1), lin-17(0), lin-17(0);mig-1(0), lin-17(1), lin-18(0), lin-18(1), lin-25(1), lin-39(2), lin-4(0), lip-1(1), LS(0), lst-1(0), lst-2(0), lst-3(0), lst-4(0), mab-5(0), mc(1), mig-1(0), mig-1(1), mig-5(1), mir-61(0), mir-61(1), mom-5(0), mom-5(1), pen-2(0), pjw5(2), pop-1(1), pop-1b(1), pry-1(0), pry-1(1), ral-1(0), ref-2(1), rgl-1(0), rVPCwt23h, sel-12(0), sel-12(1), sel-8(0), sup-17(0), sur-2(1), sys-1(0), sys-1(1), vang-1(0), vav-1(0), vav-1(1), wrm-1(1) |
| 16 | 1 | 1 | 1 | 1 | 1 | 1 | 0 | 0 |
For each mutant we obtained the cellular fates that are represented by the attractors, based on this we classified the mutants, obtaining 16 cases, and for each case we deduced the most likely phenotypes. If a worm does not have first or second fate cells, then it produces a defective vulva an it is very likely to be Egl (Cases 5-12). If the worm has no first and no second fate vulval cells then it will present a Vul phenotype (Cases 1-4). A worm which has no first fate vulval cells is also likely to be Vul (Cases 6, 7, 8), because the determination of the second fate usually depends on first fate cells, unless the second fate is determined by an alternative path. If the fusion fate is active, the worm is Vul (Even cases), a Muv phenotype is expected when only the first or second fates are possible (Cases 5, 9 and 13), when the first fate is possible but the second fate is not (Cases 9-12) Muv and Egl phenotypes are expected.