In order to further test which initiator caspase was at the apex of the apoptotic signaling, we used two clones of SW480 cells stably transfected with an expression plasmid encoding for Bcl-2.
We used eleven clones of Folsomia candida characterized by molecular markers [19] – nine from Europe (clones AP, BR, BV DK, GB, GM, HA, PB, TO) and two from North America (US, WI).
In the current study we used two clones (hIH-1 clones 1&2) of this line that were derived independently during reprogramming of the human fibroblasts.
For the data reported in Figure S2, feeding RNAi was performed as described by Kamath et al. [35], using one clone that contained a portion of the gtl-1 cDNA(656 bp) and another that contained GFP (as control).
Therefore, using four cloning systems allows the generation of four independent MAPH probe sets and subsequently a substantial increase in the number of targets that can be interrogated in a single test.
In total, we performed three independent infections of MLL-ENL cells with either control viruses or viruses encoding oncogenic RAS, using two different clones of MLL-ENL cells.
Two templates for the in vitro transcription were prepared by PCR using two separate clones (see Cloning of Distal-less section) with T7 primer and one side gene-specific primer in each (Additional file 4).
Sensitization to drug-induced apoptosis by miR-205 and miR-31 was confirmed using three independent clones of miR-205 or miR-31 stable expressing cell lines (Supplementary Figure 6C and 6D).
DOI: http://dx.doi.org/10.7554/eLife.03596.004 To confirm that the loss of INPs indeed results from the knockdown of Btd rather than off-target effects of UAS-Btd RNAi, we generated btd mutant type II NB clones using two loss-of-function alleles, btd XA and btd XG81 (Wimmer et al., 1993; Estella and Mann, 2010).
