Cyclin E2: a novel CDK2 partner in the late G1 and S phases of the mammalian cell cycle.

We report here the cloning and characterization of human and mouse cyclin E2, which define a new subfamily within the vertebrate E-type cyclins, while all previously identified family-members belong to the cyclin El subfamily. Cyclin E2/CKD2 and cyclin E/CDK2 complexes phosphorylate histone H1 in vitro with similar specific activities and both are inhibited by p27Kip1. Cyclin E2 mRNA levels in human cells oscillate throughout the cell cycle and peak at the G1/S boundary, in parallel with the cyclin E mRNA. In cells, cyclin E2 is complexed with CDK2, p27 and p21. Like cyclin E, cyclin E2 is an unstable protein in vivo and is stabilized by proteasome inhibitors. Cyclin E2-associated kinase activity rises in late G1 and peaks very close to cyclin E activity. In two malignantly transformed cell lines, cyclin E2 activity is sustained throughout S phase, while cyclin E activity has already declined and cyclin A activity is only beginning to rise. We speculate that cyclin E2 is not simply redundant with cyclin E, but may regulate distinct rate-limiting pathway(s) in G1-S control.

Telomeric repeats (TTAGGC)n are sufficient for chromosome capping function in Caenorhabditis elegans.

Telomeres are specialized structures located at the ends of linear eukaryotic chromosomes that ensure their complete replication and protect them from fusion and degradation. We report here the characterization of the telomeres of the nematode Caenorhabditis elegans. We show that the chromosomes terminate in 4-9 kb of tandem repeats of the sequence TTAGGC. Furthermore, we have isolated clones corresponding to 11 of the 12 C. elegans telomeres. Their subtelomeric sequences are all different from each other, demonstrating that the terminal TTAGGC repeats are sufficient for general chromosomal capping functions. Finally, we demonstrate that the me8 meiotic mutant, which is defective in X chromosome crossing over and segregation, bears a terminal deficiency, that was healed by the addition of telomeric repeats, presumably by the activity of a telomerase enzyme. The 11 cloned telomeres represent an important advance for the completion of the physical map and for the determination of the entire sequence of the C. elegans genome.

Anatomy and histology of aorta of White Carneau pigeon.

On the basis of anatomical and histologic studies, four distinct zones of the aorta of the atherosclerosis-prone White Carneau pigeon were defined. From its origin to about 1 cm. above the level of the celiac artery (the elastic zone), the aorta had a media composed of alternating lamellae of smooth muscle cells and fibroblasts with elastic plates between them. Distal to the elastic zone was the transitional zone, which was about 1 cm. long and ended at the level of the celiac artery. At this level there was an intimal cushion of longitudinally arranged smooth muscle cells that was present at birth but increased in thickness with age; an occasional lymphocyte-like cell was also present in the cushion. Typically, the atherosclerotic lesion originated in the smooth muscle cell cushion. In the transitional zone the media had an elastic architecture in the lateral third, the remainder being predominantly muscular. The segment of aorta from the celiac artery to the ischiadic arteries (hybrid zone) had a hybrid architecture with a thick muscular anterior wall and a thin elastic posterior wall. The structure distal to the ischiadic arteries was purely muscular (muscular zone). The presence of intimal smooth muscle cells in the transitional zone at birth, in the precise location where the "classic" atherosclerotic lesion develops months later, suggests that atherosclerosis develops within preexisting smooth muscle cell cushions which apparently represent a normal histologic feature of this area.