Chaperoning the Cln3 cyclin prevents promiscuous activation of start.

摘要

In a recent issue of Molecular Cell, Verges et al. (2007) described a new mechanism of cell-cycle control. Nuclear translocation of the G1 cyclin Cln3 is prevented by its retention at the endoplasmic reticulum (ER), and its release requires growth-associated increases in chaperone activity.