Figure 2.
Figure 2. Alterations of c-myb transcripts in OCI-Ly3. (A) Absence of c-myb transcripts initiated from the conventional promoter. PCR amplification of cDNA prepared from OCI-Ly3, HL-60, and thymus total RNA was performed with specific primers (Table 1) to detect transcripts initiated from the conventional promoter (Ex 1 + Ex 2) or the alternate promoter (Ex 1β+ Ex 2), respectively. PCR products were analyzed by agarose gel electrophoresis. While HL-60 and normal thymus contain both types of c-myb transcripts, OCI-Ly3 lacks transcripts initiated from the conventional promoter (note absence of 126-bp band). (B-D) Partial sequence of c-myb transcripts with different exon 1 sequences (ex 1, panel B; ex 1β, panel C; cryptic exon 1, panel D). The exon 1 sequence depicted in panel B is not expressed in OCI-Ly3, but that shown in panel D is OCI-Ly3 specific. The size of the first intron in each case is indicated, and the consensus splice sites are shown. The positions of the primers used in panel A also are marked. Cryptic exon 1 (panel D) is derived from the nontranscribed strand of PRDM1 intron 2 (int 2). The “intron 1” sequence for this transcript is contributed by both PRDM1 intron 2 and c-myb intron 1 sequences (Figure 1A). The 20 amino acids truncated in c-MYB in panel C and panel D are marked in bold in panel B.

Alterations of c-myb transcripts in OCI-Ly3. (A) Absence of c-myb transcripts initiated from the conventional promoter. PCR amplification of cDNA prepared from OCI-Ly3, HL-60, and thymus total RNA was performed with specific primers (Table 1) to detect transcripts initiated from the conventional promoter (Ex 1 + Ex 2) or the alternate promoter (Ex 1β+ Ex 2), respectively. PCR products were analyzed by agarose gel electrophoresis. While HL-60 and normal thymus contain both types of c-myb transcripts, OCI-Ly3 lacks transcripts initiated from the conventional promoter (note absence of 126-bp band). (B-D) Partial sequence of c-myb transcripts with different exon 1 sequences (ex 1, panel B; ex 1β, panel C; cryptic exon 1, panel D). The exon 1 sequence depicted in panel B is not expressed in OCI-Ly3, but that shown in panel D is OCI-Ly3 specific. The size of the first intron in each case is indicated, and the consensus splice sites are shown. The positions of the primers used in panel A also are marked. Cryptic exon 1 (panel D) is derived from the nontranscribed strand of PRDM1 intron 2 (int 2). The “intron 1” sequence for this transcript is contributed by both PRDM1 intron 2 and c-myb intron 1 sequences (Figure 1A). The 20 amino acids truncated in c-MYB in panel C and panel D are marked in bold in panel B.

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