Abstract
The septins are a conserved family of proteins that have been proposed to carry out diverse functions. In budding yeast, the septins become localized to the site of bud emergence in G1 but have not been thought to carry out important functions at this stage of the cell cycle. We show here that the septins function in redundant mechanisms that are required for formation of the bud neck and for the normal pattern of cell growth early in the cell cycle. The Shs1 septin shows strong genetic interactions with G1 cyclins and is directly phosphorylated by G1 cyclin-dependent kinases, consistent with a role in early cell cycle events. However, Shs1 phosphorylation site mutants do not show genetic interactions with the G1 cyclins or obvious defects early in the cell cycle. Rather, they cause an increased cell size and aberrant cell morphology that are dependent upon inhibitory phosphorylation of Cdk1 at the G2/M transition. Shs1 phosphorylation mutants also show defects in interaction with the Gin4 kinase, which associates with the septins during G2/M and plays a role in regulating inhibitory phosphorylation of Cdk1. Phosphorylation of Shs1 by G1 cyclin-dependent kinases plays a role in events that influence Cdk1 inhibitory phosphorylation.
Highlights
G1 cyclins bind and activate cyclin-dependent kinases (CDKs) to initiate cell cycle events in G1 [1,2]
A number of observations suggest that the septins function in pathways initiated by G1 cyclins to control the pattern of cell growth
Since the bud neck is formed in late G1, it seems likely that the septins execute functions when they first localize to the site of bud emergence in G1
Summary
G1 cyclins bind and activate cyclin-dependent kinases (CDKs) to initiate cell cycle events in G1 [1,2]. An important function of the G1 cyclins is to initiate growth of a new daughter cell [3,4,5,6]. There are two CDKs that function during G1 in budding yeast, called Cdk and Pho, which are activated by numerous different cyclins [1]. Cdk is activated by Cln, Cln, and Cln, while Pho is activated by Pcl and Pcl, as well as a number of additional cyclins that do not appear to directly regulate G1 events. Loss of Cln or Cln and Cln causes delayed initiation of bud growth, but loss of all three cyclins leads to a failure to initiate bud growth [4,5]. The extensive redundancy of G1 cyclins implies the existence of multiple overlapping pathways that control G1 events
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