DEV008821 Supplementary Material

Files in this Data Supplement:

• Supplemental Table S1 -

  Table S1. Phenotypes of muscles DO3 and DT1 in individual hemisegments of Poxm and l(1)sc; Poxm mutants. Mutant phenotypes, analyzed as described in the legend to Fig. 5, are given for muscles DO3 and DT1 of individual hemisegments, as summarized in Fig. 5A,D. Each line lists the phenotypes of a hemisegment for muscles DO3 and DT1 of Poxm^R361 mutants (left column, 108 hemisegments) and of Df(1)sc¹⁹/Df(1)sc¹⁹ or Y; Poxm^R361 mutants (right column, 168 hemisegments). Muscle phenotypes were classified as missing (M, red), abnormal (A, yellow), duplicated (D, purple) and normal wild type (N, green).

• Supplemental Figure S1 -

  Fig. S1. Structural organization of the Poxm gene and Poxm protein sequence. (A) Overlapping DNA fragments, covering the Poxm locus, P29, P20, P106 and P111, and isolated from a genomic library in λ phage EMBL4 (Bopp et al., 1989), are shown at the top with respect to an EcoRI restriction map below, in which the location of the P-element insertion P282 (Deák et al., 1997) is indicated. The locations and orientations of the two Poxm exons (Bopp et al., 1989), shown below the restriction map, were derived by sequencing of two Poxm cDNAs, P29c1 and P29c2, differing mainly in the lengths of their trailers, and of the corresponding genomic DNA, whereas the transcriptional start site was determined by 5′ RACE and coincides with the 5′ end of P29c1 (the GenBank accession number for the full-length Poxm cDNA P29c1, is DQ459353; for P29c2 it is DQ459354). The exons corresponding to the full-length Poxm transcript indicate the open reading frame (shaded) with the paired-domain (black), the untranslated leader and trailer (white), and two different poly(A) addition sites found in two cDNAs (vertical marks). Two deficiencies, Df(3R)159 and Df(3R)dsx^D+R5, are indicated at the bottom. Whereas their proximal breakpoints map proximal to the genomic region shown, their distal breakpoints are located within the regions delimited by the open boxes. (B) Amino acid sequence of Poxm derived from the longest open reading frame of Poxm cDNAs. The previously published paired-domain and octapeptide (Bopp et al., 1989; Noll, 1993) are underlined, and the location of the EMS-induced amber mutation Poxm³⁶¹, Q15stop, is indicated by an arrow. The black triangle marks the position of the intron. Note that amino acids 5-370 are identical to 37-402 of the Poxm protein published by FlyBase, whereas our N-terminal amino acids deviate because the first exon has been incorrectly predicted by FlyBase.

• Supplemental Figure S2 -

  Fig. S2. lacZ expressed under the direct control of the Poxm enhancers coincides with endogenous Poxm protein. Transgenic embryos at early stage 11, expressing lacZ under the direct control of the 1.8 kb fragment (A-C) or the 8.4 kb fragment (D-F), both including the early enhancer of Poxm (Fig. 3E), were stained for Poxm (A,D) and β-gal (B,E). The two expression patterns completely coincide, and no ectopic β-gal is observed (C,F). Note that Poxm is nuclear whereas β-gal is cytoplasmic.