We describe here the cloning of the Aplysia K+ channel AK01a.AK01a codes for a protein of 515 amino acids, shows considerable homology to other cloned potassium channels, and can be classified as a member of the ShakerK+ channel family. Expression of the AK01a channel in Xenopus oocytes produces a rapidly inactivating outward potassium current (IAK01a) resembling the A-type currents of Drosophila Shaker. Gating for this current is shifted to potentials considerably more positive than the traditional A-currents of Aplysia; we have, however, identified a novel transient potassium current (IAdepoI) in a subset of Aplysia neurons that has similar gating and pharmacological properties to IAK01a.

Activation of the mouse c-myb oncogene in Abelson virus-induced plasmacytoid lymphosarcomas was studied using cDNA cloning and nucleotide sequence analysis. The results presented here show that viral integration in the myb locus generates splicing errors at the 5' and 3' regions. Viral integration results in transcriptional initiation within the viral long terminal repeat and generation of a chimeric mRNA that lacks the rst three coding exons. The alterations at the 3' end are caused by an aberrant splicing event in which additional splice-donor and -acceptor sequences within intronic sequences are used to splice an additional 363 nucleotides into the myb transcripts. The resulting insertion of 121 amino acids is in a region of the protein where other activated forms of the myb gene product have deletions. These results suggest that alterations in the 3' end of the myb gene play a crucial role in the activation of this gene.A comparative study of retroviral oncogenes and their cellular homologues has given us invaluable information regarding the structural changes that protooncogenes often undergo to acquire transforming potential. A comparison of the c-myb cDNA sequence (1) with the v-myb sequence of avian myeloblastosis virus (AMV) (2, 3) and E26 leukemia virus (4) revealed that large stretches of coding sequences from the 5' and 3' ends have been deleted during the transduction of this gene into the viral genome. The AMV myb gene is derived from seven of the internal coding exons of the c-myb gene (3, 5) and has undergone deletions of 142 amino acids at its N-terminal end and 192 amino acids at its C-terminal end (1). Similar deletions have occurred in the E26 virus, in which myb is coded as part of a fusion polypeptide of three distinct elements, the viral gag sequences, the viral myb, and a third element derived from the protooncogene ets (4). Deletions of similar stretches of sequences in two independent viral isolates suggest that these deletions are important for the oncogenic activation of the myb gene.Another model system that has allowed us to study the activation of the myb gene is the Abelson leukemia virusinduced plasmacytoid lymphosarcomas (ABPL tumors) of the mouse (6). Detailed analysis ofthese tumors revealed that they do not contain the integrated Abelson leukemia virus genome, but instead have undergone rearrangements in their myb locus as a result of Moloney murine leukemia virus (Mo-MuLV) integration (5,7,8).To study the effect of the viral integration on the transcription of the rearranged myb locus in ABPL tumors, we have undertaken the cDNA cloning of myb mRNA from one of the ABPL tumors, ABPL-2, and determined its sequence. Our results show that the viral integration results in aberrant splicing events at both the 5' and 3' ends of the mRNA transcripts producing alterations in similar positions to those seen in AMV and E26 virus.

The productively rearranged immunoglobulin mu chain gene and the translocated cellular oncogene c-myc are transcribed at high levels both in human Burkitt lymphoma cells carrying the t(8;14) chromosome translocation and in mouse plasmacytoma X Burkitt lymphoma cell hybrids. In the experiments reported here these genes were found to be repressed in mouse 3T3 fibroblast X Burkitt lymphoma cell hybrids. Such repression probably occurs at the transcriptional level since no human mu- and c-myc messenger RNA's are detectable in hybrid clones carrying the corresponding genes. It is therefore concluded that the ability to express these genes requires a differential B cell environment. The results suggest that the 3T3 cell assay may not be suitable to detect oncogenes directly involved in human B cell oncogenesis, since 3T3 cells apparently are incapable of transcribing an oncogene that is highly active in malignant B cells with specific chromosomal translocations.

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