DEV02748 Supplementary Material

Files in this Data Supplement:

• Supplemental Figure 1 -

  Fig. S1. The molecular lesion in the null allele abl⁴. (A) Schematic of the abl⁴ molecular lesion. A deletion in the region coding for the SH2 domain results in a frameshift, leading to a premature truncation. Sequence analysis shows that the abl⁴ deletion removes 23 nucleotides, including four nucleotides of the exon, the 5′ splice site (GT) of the 3rd intron. Note that, if the next ‘GT’ were used for splicing in abl⁴, Leu309 Arg310 would be replaced with Ser, and theoretically a nearly full-length protein would be produced. However, we did not detect any spliced product in RT-PCR (data not shown), and we did not detect a near-full-length protein in abl⁴ mutants (see lane 3 in B). (B) Confirmation of rescue by Abl::GFP. Abl immunoblot from adult flies. Lane 1, wild type. Lane 2, Abl::GFP transgene in wild type. Lane 3, Abl::GFP transgene in abl¹/abl⁴. Note wild-type Abl at ∼180 kDa in wild-type (lane 1), wild-type and higher molecular weight, GFP-tagged-Abl in Abl::GFP transgenics (lane 2), and only GFP-tagged Abl when the transgene is crossed into an abl¹/abl⁴ background (lane 3). Note that, as there is no band approximately the size of wild-type Abl, this suggests that cryptic splicing from a downstream ‘GT’ does not produce a nearly full-length protein in abl⁴.

• Movie 1 -

  Movie 1. Wild-type ventral furrow formation, moesin::GFP. One frame=15 seconds. Stills from movie are in Fig. 1Q. See text for details.

• Movie 2 -

  Movie 2. abl mutant ventral furrow formation, moesin::GFP. One frame=15 seconds. Stills from movie are in Fig. 1R. See text for details.