Figure 2.

(A) Southern hybridization of genomic DNA from the Charolles parental strain (Ch) carrying the rl⁺ allele, and from rl^IR1 homozygotes (rl^IR), digested with EcoRI and probed with the 1.4-kb rl cDNA probe (30); black arrows indicate the bands whose mobility varies in the rl^IR1 mutant and in the Charolles strain. (B) Filters were stripped and reprobed with I sequences; the open arrow indicates I-homologous sequences in the dysgenic mutants that comigrate with rl homologous sequences. (C) Southern hybridization of genomic DNA from Canton-S (C) and Charolles (Ch) parental stains carrying the rl⁺ allele, and from rl^IR1 homozygotes (rl^IR), digested with EcoRV and probed with the HindIII–DraI fragment. (D) PCR amplification reaction from genomic DNA of Canton-S (C), Charolles (Ch), and rl^IR1 strains. A 982-bp fragment was specifically amplified from genomic DNA of rl^IR1 homozygotes. M, molecular weight marker. (E) Northern blot assays of second-instar larvae total RNA from rl⁺, rl^IR1, and Df(2Rh)Rspⁱ¹ homozygotes lacking the rl gene. The 1.4-kb rl cDNA probe reveals two major transcripts of 2.6 kb and 1.9 kb, both absent in larvae homozygous for Df(2Rh)Rspⁱ¹. The same filter was reprobed with the rp49 ribosomal protein gene probe as a loading control.