dcp-66 : pgp-11

RNAi against dcp-66 showed a substantial inhibition of GFP expression driven by DH11.3 promoter which contains the Ex-1 (10-bp element that drives excretory cell-specific expression).

F48E8.3 : dcp-66

RNAi against dcp-66 showed a substantial inhibition of GFP expression driven by F48E8.3 promoter which contains the Ex-1 (10-bp element that drives excretory cell-specific expression).

dcp-66 : inx-13

RNAi against dcp-66 showed a substantial inhibition of GFP expression driven by Y8G1A.2 promoter which contains the Ex-1 (10-bp element that drives excretory cell-specific expression).

dcp-66 : pgp-12

RNAi against dcp-66 showed a substantial inhibition of GFP expression driven by pgp-12 promoter which contains the Ex-1 (10-bp element that drives excretory cell-specific expression).

Transcription factor binding site : ssu-1

The deletion or the mutation of the individual 6 bp elements of the ASJ motif in the ssu-1 promoter robustly decreases gene ex- pression in ASJ, indicating that the ASJ motif is also functional in ssu-1.

Transcription factor binding site : ssu-1

The deletion or the mutation of the individual 6 bp elements of the ASJ motif in the ssu-1 promoter robustly decreases gene ex- pression in ASJ, indicating that the ASJ motif is also functional in ssu-1.

LIN-1 binding site : egl-1

When the LIN-1 recognition sequence CAGGAA in the P3 region of the egl-1 promoter was mutated into GCTACT [65], the mutant egl-1 transgene Ex[egl-1(mut)] only partially rescued the egl-1 cell death defect. In the two transgenic lines, the percentages of ABpl/rpppapp survival were 15% and 25%, similar to that of the lin-3 mutant. The egl-1; Ex[egl-1(mut)] transgenic worms also had a similar number of embryonic cell corpses as the lin-3 mutant at the 1.5-fold stage. These results show that the binding of LIN-1 to the egl-1 promoter is important for the cell-killing activity of egl-1.

Y48G1A.8 : che-2 : daf-25

chb-3 suppresses the small body size of che-3; however, the body-size of the double mutant was not significantly different from the large body-size of chb-3 single mutants. Body-size of the double mutant was not influenced by the addition of more che-2 through expression o transgene Ex[che-2].

end-3 : ref-1

In end-3(-) embryos as a result of the abnormal proximity to MSapp, ref-1 reporter expression can be increased in Ear daughters compared to wild type and in turn ref-1 reporter expression in Epl daughters can be decreased. These levels are negatively correlated with the distance of the cell from MSapp. In end-3(-) embryos the expression of ref-1 had a partially penetrant increase in the daughters of the Ear cell associated 306 with a corresponding decrease in the daughters of the Epl cells. We hypothesize that atypical divisions at the Ex stage in end-3(-) embryos result in this ectopic expression.

syg-1 : syg-2

To ask whether SYG-2 directly specifies the location of SYG-1 and synaptic vesicles, SYG-2 was expressed in secondary vulval epithelial cells using an egl-17 promoter in syg-2(ky673) mutants. In wild-type early L4 stage animals, the primary vulval epithelial cells expressed SYG-2::GFP, the HSN axon contacted the ventral edge of the two most ventral primary vulval epithelial cells, and SYG-1 in HSNL was localized to the contact sites between the HSNL axon and the primary vulval cells. In syg-2 mutants, SYG-1 was evenly distributed on the HSNL axon. In syg-2(ky673); Ex(egl-17::syg-2) animals, syg-2 should be expressed in the secondary vulval cells but not the primary vulval cells. In these animals, SYG-1 in HSNL was localized to the contact sites between HSNL and the ventral secondary vulval cells. These results suggest that SYG-2 expression in the secondary vulval cells is sufficient to attract SYG-1 protein from the HSNL axon.