Abstract
AbstractEntry into the cell cycle in late G1 phase occurs only when sufficient growth has occurred. In budding yeast, a cyclin called Cln3 is thought to link cell cycle entry to cell growth. Cln3 accumulates during growth in early G1 phase and eventually triggers accumulation of late G1 cyclins that drive cell cycle entry. All current models assume that Cln3 works solely in G1 phase and activates Cdk1 to initiate accumulation of late G1 cyclins solely via transcriptional mechanisms. Here, we show that Cln3 can influence accumulation of late G1 cyclin proteins via post-transcriptional mechanisms. Furthermore, proteomic analysis of the effects of loss- or gain-of-function of Cln3 found no clear evidence that Cln3 activates Cdk1, and an analysis of Cln3 binding to Cdk1 failed to find clear evidence that Cln3 can bind directly to Cdk1, which suggests that Cln3 could carry out functions independently of Cdk1, similar to mammalian cyclin F. Finally, we show that Cln3 has functions in mitosis that strongly influence cell size. Together, these discoveries reveal surprising new functions for Cln3 that challenge current models for control of cell cycle entry and cell size.
Publisher
Cold Spring Harbor Laboratory