No abstract

The presence and synthesis of c‐myc protein and mRNA in the cell cycle has been studied. We find that c‐myc mRNA is present, at equivalent levels, at all times in the cell cycle with the possible exception of mitosis. Furthermore, we demonstrate that this mRNA is transcribed in both G1 and G2 phases. An analysis of the c‐myc protein in vivo shows that de novo synthesis occurs in G1 and G2 and the protein turns over with a half‐life of approximately 20‐30 min in both phases. Furthermore, the level of c‐myc protein rapidly increases in cell populations when they re‐initiate the cell cycle, thereafter decreasing as the culture reaches quiescence. The results therefore suggest that expression of c‐myc can be rapidly modulated and that it is activated during the G0 to G1 transition, but is expressed thereafter in the cell cycle.

The human c-myc gene consists of three exons transcribed from two distinct promoters and the function of the first, noncoding exon is unknown. In COLO 320 cells, there co-exist normal and truncated (i.e., lacking exon 1) c-myc genes, both of which are transcribed. Studies on the turnover of c-myc mRNA show that the normal mRNA has an in vivo half-life of -30 min which is approximately similar to the turnover time of the mRNA in lymphoblastoid cells. However, the truncated mRNA was found to be substantially more stable. This observation was also made with a Burkitt's lymphoma cell line which has a translocated, truncated c-myc gene. Therefore truncation of the c-myc gene can cause the mRNA to be more stable than the full size product suggesting that this can be a crucial factor in the activation of the c-myc oncogene, by exon 1 loss, in chromosomal translocation. The results also suggest a role for exon 1 in the c-myc mRNA degradative mechanism.

We have examined the chromosomal location of human T cell‐specific genes which are involved in antigen recognition and of a gene which specifically rearranges in T cells. The genes encoding both the variable and constant region segments of the T cell receptor alpha chain are found on chromosome 14 while the delta chain gene of the T cell receptor‐associated T3 complex is localised to chromosome 11. Further, the two tandemly arranged T cell‐specific rearranging genes, designated gamma, were mapped to chromosome 7, but apparently not closely linked to the previously mapped T cell receptor beta‐chain gene. The locations of the three different genes, which undergo rearrangement in T cells, may correlate with the chromosomal breakpoints known to be involved in translocations within abnormal human T cells.

No abstract